Tokushima University / Educator and Researcher Directory --- Murakami, Keiji

Personal Web Page

https://researchmap.jp/read0088249 (researchmap)

Field of Study

○	Microbiology

Subject of Study

○	ストレス反応が及ぼす抗菌薬抵抗性への影響について (緑膿菌, 抗菌薬抵抗性, バイオフィルム)

Book / Paper

Book:

1.	Hiromichi Yumoto, Katsuhiko Hirota, Kouji Hirao, Masami Ninomiya, Keiji Murakami, Hideki Fujii and Yoichiro Miyake : The Pathogenic Factors from Oral Streptococci for Systemic Diseases, Aug. 2020.
2.	Keiji Murakami : Streptococcus pseummoniae, 2014.
3.	Peterson SB, Irie Y, Borlee BR, Keiji Murakami, Harrison JJ, Colvin KM and Parsek MR : Different methods for culturing biofilms in vitro, 2011.

Academic Paper (Judged Full Paper):

1.	Adityakrisna Putra Yoshi Wigianto, Yuichi Ishida, Yuki Iwawaki, Takaharu Goto, Megumi Watanabe, Kazumitsu Sekine, Kenichi Hamada, Keiji Murakami, Hideki Fujii and Tetsuo Ichikawa : 2-methacryloyloxyethyl phosphorylcholine polymer treatment prevents Candida albicans biofilm formation on acrylic resin, Journal of Prosthodontic Research, Vol.67, No.3, 384-391, 2022. (Summary) We aimed to evaluate the effectiveness of photoreactive 2-methacryloyloxyethyl phosphorylcholine (MPC) in inhibiting Candida albicans biofilm formation on polymethyl methacrylate (PMMA) and assess its mechanism and need for re-application by evaluating its interaction with salivary mucin and durability during temperature changes. PMMA discs were used as specimens. The MPC coating was applied using the spray and cure technique for the treatment groups, whereas no coating was applied to the control. The MPC treatment (MT) groups were further differentiated based on the number of thermal cycles involved (0, 1000, 2500, and 5000). The optical density was measured to assess mucin adsorption (MA). Contact angle (CA) was calculated to evaluate surface hydrophilicity. The presence of MPC components on the PMMA surface was assessed using X-ray photoelectron spectroscopy (XPS). C. albicans biofilms were evaluated qualitatively (scanning electron microscope images) and quantitatively (colony-forming units (CFUs)). Statistical analysis was conducted using two-way analysis of variance and Tukey's multiple comparison test. MA rate and CA increased significantly in the MT groups, which exhibited significantly fewer CFUs and thinner biofilms than those of the control group. Based on the XPS, MA, and CFU evaluations, the durability and efficacy of the MPC coating were considered stable up to 2500 thermal cycles. Additionally, a significant interaction was observed between mucin concentration and MPC efficacy. The photoreactive MPC coating, which was resistant to temperature changes for approximately 3 months, effectively prevented C. albicans biofilm formation by modifying surface hydrophilicity and increasing mucin adsorption. (Keyword) Candida albicans / Acrylic Resins / Polymers / Polymethyl Methacrylate / Surface Properties / Biofilms / Mucins (Tokushima University Institutional Repository) ● Metadata: 119402 (Link to Publication Site) ● Publication site (DOI): 10.2186/jpr.JPR_D_22_00102 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36288959 ● Summary page in Scopus @ Elsevier: 2-s2.0-85166383313 (Tokushima University Institutional Repository: 119402, DOI: 10.2186/jpr.JPR_D_22_00102, PubMed: 36288959, Elsevier: Scopus)
2.	Yuta Uemura, Yuka Hiroshima, Ayano Tada, Keiji Murakami, Kaya Yoshida, Yuji Inagaki, Tomomi Kuwahara, Akikazu Murakami, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways, Biomedicines, Vol.10, No.10, 2643, 2022. (Summary) () is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. -OMVs are involved in the pathogenesis of periodontitis. -OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of -OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. -OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. -OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that -OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that -OMVs may play important roles in periodontitis exacerbation by stimulating various pathways. (Tokushima University Institutional Repository) ● Metadata: 117616 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10102643 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36289904 ● Search Scopus @ Elsevier (PMID): 36289904 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10102643 (Tokushima University Institutional Repository: 117616, DOI: 10.3390/biomedicines10102643, PubMed: 36289904)
3.	Muhammad Reza Pahlevi, Keiji Murakami, Yuka Hiroshima, Akikazu Murakami and Hideki Fujii : pruR and PA0065 Genes Are Responsible for Decreasing Antibiotic Tolerance by Autoinducer Analog-1 (AIA-1) in Pseudomonas aeruginosa, Antibiotics, Vol.11, No.6, 773, 2022. (Tokushima University Institutional Repository) ● Metadata: 117279 (Link to Publication Site) ● Publication site (DOI): 10.3390/antibiotics11060773 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35740179 ● Search Scopus @ Elsevier (PMID): 35740179 ● Search Scopus @ Elsevier (DOI): 10.3390/antibiotics11060773 (Tokushima University Institutional Repository: 117279, DOI: 10.3390/antibiotics11060773, PubMed: 35740179)
4.	Akihiro Wada, Keiji Murakami, Yumi Ishikawa, Takashi Amoh, Kouji Hirao, Yuki Hosokawa, Daisuke Hinode, Yoichiro Miyake and Hiromichi Yumoto : Anti-Inflammatory and Protective Effects of Juncus effusus L. Water Extract on Oral Keratinocytes, BioMed Research International, Vol.2022, 9770899, 2022. (Summary) Periodontitis is a chronic inflammatory disease caused by periodontopathogenic bacteria that form biofilms in periodontal pockets. The gingival epithelium acts as the first physical barrier in fighting attacks by periodontopathogenic pathogens, such as the primary etiological agent , and various exogenous chemicals, as well as regulates the local innate immune responses. Therefore, the development of novel oral care products to inhibit inflammatory reactions caused by bacterial infection and protect the gingival epithelium is necessary. L. has generally been used as an indigenous medicine, such as a diuretic, an antipyretic, and an analgesic, in ancient practice. In this study, we examined the effects of a water extract from L. on the inhibition of the inflammatory reaction elicited by bacterial infection and protection of the oral epithelium by chemical irritation. Pretreatment of oral epithelial cells with the water extract from L. significantly reduced or its lipopolysaccharide- (LPS-) mediated production of chemokines (interleukin-8 and C-C-chemokine ligand20) in a concentration-dependent manner with comparable to or greater effects than epigallocatechin gallate and protected oral epithelial cells from injury by chemical irritants, cetylpyridinium chloride, and benzethonium chloride. Moreover, the water extract from . L. in the presence of antimicrobial agents or antifibrinolytics already used as ingredients in mouthwash could significantly reduce the production of chemokines from LPS-stimulated oral epithelial cells in a concentration-dependent manner. These findings suggest that the water extract from . L. is potentially useful for oral care to prevent oral infections, such as periodontal infections, and maintain oral epithelial function. (Keyword) Anti-Inflammatory Agents / Bacteroidaceae Infections / Cell Line, Transformed / Humans / Keratinocytes / Magnoliopsida / Mouth Mucosa / Periodontitis / Plant Extracts / Porphyromonas gingivalis (Tokushima University Institutional Repository) ● Metadata: 117031 (Link to Publication Site) ● Publication site (DOI): 10.1155/2022/9770899 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35028318 ● Summary page in Scopus @ Elsevier: 2-s2.0-85123567270 (Tokushima University Institutional Repository: 117031, DOI: 10.1155/2022/9770899, PubMed: 35028318, Elsevier: Scopus)
5.	Mizuki Abe, Keiji Murakami, Yuka Hiroshima, Takashi Amoh, Mayu Sebe, Keiko Kataoka and Hideki Fujii : Autoinducer Analogs Can Provide Bactericidal Activity to Macrolides in Pseudomonas aeruginosa through Antibiotic Tolerance Reduction, Antibiotics, Vol.11, No.1, 2021. (Summary) Macrolide antibiotics are used in treating chronic biofilm infections despite their unsatisfactory antibacterial activity, because they display several special activities, such as modulation of the bacterial quorum sensing and immunomodulatory effects on the host. In this study, we investigated the effects of the newly synthesized quorum-sensing autoinducer analogs (AIA-1, -2) on the activity of azithromycin and clarithromycin against . In the killing assay of planktonic cells, AIA-1 and -2 enhanced the bactericidal ability of macrolides against PAO1; however, they did not affect the minimum inhibitory concentrations of macrolides. In addition, AIA-1 and -2 considerably improved the killing activity of azithromycin and clarithromycin in biofilm cells. The results indicated that AIA-1 and -2 could affect antibiotic tolerance. Moreover, the results of hydrocarbon adherence and cell membrane permeability assays suggested that AIA-1 and -2 changed bacterial cell surface hydrophobicity and accelerated the outer membrane permeability of the hydrophobic antibiotics such as azithromycin and clarithromycin. Our study demonstrated that the new combination therapy of macrolides and AIA-1 and -2 may improve the therapeutic efficacy of macrolides in the treatment of chronic biofilm infections. (Tokushima University Institutional Repository) ● Metadata: 117210 (Link to Publication Site) ● Publication site (DOI): 10.3390/antibiotics11010010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35052885 ● Summary page in Scopus @ Elsevier: 2-s2.0-85121669540 (Tokushima University Institutional Repository: 117210, DOI: 10.3390/antibiotics11010010, PubMed: 35052885, Elsevier: Scopus)
6.	Momoyo Azuma, Keiji Murakami, Rina Murata, Keiko Kataoka, Hideki Fujii, Yoichiro Miyake and Yasuhiko Nishioka : Clinical Significance of Carbapenem-Tolerant Pseudomonas aeruginosa Isolated in the Respiratory Tract, Antibiotics, Vol.9, No.9, 2020. (Summary) infections. (Tokushima University Institutional Repository) ● Metadata: 116480 (Link to Publication Site) ● Publication site (DOI): 10.3390/antibiotics9090626 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32967210 ● Search Scopus @ Elsevier (PMID): 32967210 ● Search Scopus @ Elsevier (DOI): 10.3390/antibiotics9090626 (Tokushima University Institutional Repository: 116480, DOI: 10.3390/antibiotics9090626, PubMed: 32967210)
7.	Natsumi Fujiwara, Keiji Murakami, Kaya Yoshida, Shunsuke Sakurai, Yasusei Kudo, Kazumi Ozaki, Katsuhiko Hirota, Hideki Fujii, Maiko Suzuki, Yoichiro Miyake and Hiromichi Yumoto : Suppresive effects of 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymer on the adherence of Candida species and MRSA to acrylic denture resin., Heliyon, Vol.6, e04211, 2020. (Tokushima University Institutional Repository) ● Metadata: 115916 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.heliyon.2020.e04211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32577575 ● Summary page in Scopus @ Elsevier: 2-s2.0-85086425832 (Tokushima University Institutional Repository: 115916, DOI: 10.1016/j.heliyon.2020.e04211, PubMed: 32577575, Elsevier: Scopus)
8.	Natsumi Fujiwara, Hiromichi Yumoto, Koji Miyamoto, Katsuhiko Hirota, Hiromi Nakae, Saya Tanaka, Keiji Murakami, Yasusei Kudo, Kazumi Ozaki and Yoichiro Miyake : 2-Methacryloyloxyethyl phosphorylcholine (MPC)-polymer suppresses an increase of oral bacteria: a single-blind, crossover clinical trial, Clinical Oral Investigations, Vol.23, 739-746, 2019. (Summary) The biocompatible 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymers, which mimic a biomembrane, reduce protein adsorption and bacterial adhesion and inhibit cell attachment. The aim of this study is to clarify whether MPC-polymer can suppress the bacterial adherence in oral cavity by a crossover design. We also investigated the number of Fusobacterium nucleatum, which is the key bacterium forming dental plaque, in clinical samples. This study was a randomized, placebo-controlled, single-blind, crossover study, with two treatment periods separated by a 2-week washout period. We conducted clinical trial with 20 healthy subjects to evaluate the effect of 5% MPC-polymer mouthwash after 5 h on oral microflora. PBS was used as a control. The bacterial number in the gargling sample before and after intervention was counted by an electronic bacterial counter and a culture method. DNA amounts of total bacteria and F. nucleatum were examined by q-PCR. The numbers of total bacteria and oral streptcocci after 5 h of 5% MPC-polymer treatment significantly decreased, compared to the control group. Moreover, the DNA amounts of total bacteria and F. nucleatum significantly decreased by 5% MPC-polymer mouthwash. We suggest that MPC-polymer coating in the oral cavity may suppress the oral bacterial adherence. MPC-polymer can be a potent compound for the control of oral microflora to prevent oral infection. (Keyword) 2-Methacryloyloxyethylphosphorylcholine / Clinical study / Oral infection / Oral bacteria / Fusobacterium nucleatum (Tokushima University Institutional Repository) ● Metadata: 113011 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00784-018-2490-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29766378 ● Summary page in Scopus @ Elsevier: 2-s2.0-85046904798 (Tokushima University Institutional Repository: 113011, DOI: 10.1007/s00784-018-2490-2, PubMed: 29766378, Elsevier: Scopus)
9.	Hiromichi Yumoto, Katsuhiko Hirota, Kouji Hirao, Masami Ninomiya, Keiji Murakami, Hideki Fujii and Yoichiro Miyake : The pathogenic factors from oral Streptococci for systemic diseases, International Journal of Molecular Sciences, Vol.20, No.18, 2019. (Tokushima University Institutional Repository) ● Metadata: 114574 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms20184571 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85072542634 (Tokushima University Institutional Repository: 114574, DOI: 10.3390/ijms20184571, Elsevier: Scopus)
10.	Susilowati Heni, Keiji Murakami, Hiromichi Yumoto, Takashi Amoh, Kouji Hirao, Katsuhiko Hirota, Takashi Matsuo and Yoichiro Miyake : Royal jelly inhibits Pseudomonas aeruginosa adherence and reduces excessive inflammatory responses in human epithelial cells, BioMed Research International, Vol.2017, 3191752, 2017. (Summary) is a Gram-negative bacterium and causes respiratory infection especially in elderly patients. Royal jelly has been used worldwide as a traditional remedy and as a nutrient; however, the effect against is unclear. The aim of this study was to analyze antibacterial, antiadherent, and anti-inflammatory effects of royal jelly against . Wild-type strain PAO1 and clinical isolates of were used for antibacterial assay and antiadherent assay to abiotic surface and epithelial cells, which are pharynx (Detroit 562) and lung (NCI-H292) epithelial cells. In anti-inflammatory assay, epithelial cells were pretreated with royal jelly before bacterial exposure to investigate its inhibitory effect on interleukin (IL-8) and macrophage inflammatory protein-3/CCL20 overproduction. Although royal jelly did not have antibacterial activity at concentration of 50% w/v, antiadherent activity was confirmed on the abiotic surface and epithelial cells under concentration of 25%. Pretreatment with royal jelly significantly inhibited overproduction of IL-8 and CCL20 from both cells. These results demonstrated that royal jelly inhibits adherence and protects epithelial cells from excessive inflammatory responses against infection. Our findings suggested that royal jelly may be a useful supplement as complementary and alternative medicine for preventing respiratory infection caused by . (Keyword) Cell Line / Chemokine CCL20 / Epithelial Cells / Fatty Acids / Gene Expression Regulation / Humans / inflammation / Interleukin-8 / Pseudomonas Infections / Pseudomonas aeruginosa (Tokushima University Institutional Repository) ● Metadata: 112385 (Link to Publication Site) ● Publication site (DOI): 10.1155/2017/3191752 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29075644 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030761989 (Tokushima University Institutional Repository: 112385, DOI: 10.1155/2017/3191752, PubMed: 29075644, Elsevier: Scopus)
11.	Sekita Yasuko, Keiji Murakami, Hiromichi Yumoto, Kouji Hirao, Takashi Amoh, Natsumi Fujiwara, Katsuhiko Hirota, Hideki Fujii, Takashi Matsuo, Yoichiro Miyake and Yoshiki Kashiwada : Antibiofilm and Anti-Inflammatory Activities of+ Houttuynia cordata Decoction for Oral Care, Evidence-Based Complementary and Alternative Medicine : eCAM, Vol.2017, 2850947, 2017. (Summary) Dental biofilms that form in the oral cavity play a critical role in the pathogenesis of several infectious oral diseases, including dental caries, periodontal disease, and oral candidiasis. (HC, Saururaceae) is a widely used traditional medicine, for both internal and external application. A decoction of dried HC leaves (dHC) has long been consumed as a health-promoting herbal tea in Japan. We have recently reported that a water solution of HC poultice ethanol extract (wHCP) exerts antimicrobial and antibiofilm effects against several important oral pathogens. It also exhibits anti-inflammatory effects on human keratinocytes. In our current study, we examined the effects of dHC on infectious oral pathogens and inflammation. Our results demonstrated that dHC exerts moderate antimicrobial effects against methicillin-resistant (MRSA) and other oral microorganisms. dHC also exhibited antibiofilm effects against MRSA, (involved in dental plaque formation), and and inhibitory effects on interleukin-8, CCL20, IP-10, and GRO productions by human oral keratinocytes stimulated by lipopolysaccharide (a cause of periodontal disease), without cytotoxic effects. This suggests that dHC exhibits multiple activities in microorganisms and host cells. dHC can be easily prepared and may be effective in preventing infectious oral diseases. (Tokushima University Institutional Repository) ● Metadata: 112956 (Link to Publication Site) ● Publication site (DOI): 10.1155/2017/2850947 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29234378 ● Summary page in Scopus @ Elsevier: 2-s2.0-85042323475 (Tokushima University Institutional Repository: 112956, DOI: 10.1155/2017/2850947, PubMed: 29234378, Elsevier: Scopus)
12.	Takashi Amoh, Keiji Murakami, Kariyama Reiko, Hori Kenji, Vidoucic Darija, Katsuhiko Hirota, Igarashi Jun, Suga Hiroaki, Pasek R Matthew, Kumon Hiromi and Yoichiro Miyake : Effects of an autoinducer analogue on antibiotic tolerance in Pseudomonas aeruginosa, The Journal of Antimicrobial Chemotherapy, Vol.72, No.8, 2230-2240, 2017. (Summary) Antibiotic tolerance causes chronic, refractory and persistent infections. In order to advance the development of a new type of drug for the treatment of infectious diseases, we herein investigated the effects of a newly synthesized analogue of the Pseudomonas aeruginosa quorum-sensing autoinducer named AIA-1 ( a uto i nducer a nalogue) on antibiotic tolerance in P. aeruginosa . A P. aeruginosa luminescent strain derived from PAO1 was injected into neutropenic ICR mice and bioluminescence images were acquired for a period of time after treatments with antibiotics and AIA-1. In vitro susceptibility testing and killing assays for the planktonic and biofilm cells of PAO1 were performed using antibiotics and AIA-1. The expression of quorum-sensing-related genes was examined using real-time PCR. In vivo and in vitro assays showed that AIA-1 alone did not exert any bactericidal effects and also did not affect the MICs of antibiotics. However, the combined use of AIA-1 and antibiotics exerted markedly stronger therapeutic effects against experimental infection than antibiotics alone. The presence of AIA-1 also enhanced the killing effects of antibiotics in planktonic and biofilm cells. Although AIA-1 did not inhibit the expression of lasB and rhlA genes, which are directly regulated by quorum sensing, it clearly suppressed expression of the rpoS gene. The new compound, AIA-1, did not alter the antibiotic susceptibility of P. aeruginosa by itself; however, its addition enhanced the antibacterial activity of antibiotics. AIA-1 did not inhibit quorum sensing, but reduced the antibiotic tolerance of P. aeruginosa by suppressing rpoS gene expression. (Link to Publication Site) ● Publication site (DOI): 10.1093/jac/dkx132 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28510695 ● Search Scopus @ Elsevier (PMID): 28510695 ● Search Scopus @ Elsevier (DOI): 10.1093/jac/dkx132 (DOI: 10.1093/jac/dkx132, PubMed: 28510695)
13.	Natsumi Fujiwara, Keiji Murakami, Michiyasu Nakao, Munehisa Toguchi, Hiromichi Yumoto, Katsuhiko Hirota, Takashi Matsuo, Shigeki Sano, Kazumi Ozaki and Yoichiro Miyake : Antibacterial and antibiofilm effects of Reuterin-Related Compounds to periodontopathic bacteria, Journal of Oral Health and Biosciences, Vol.30, No.1, 8-17, 2017. (Tokushima University Institutional Repository) ● Metadata: 111063 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.30.1_8 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.30.1_8 (Tokushima University Institutional Repository: 111063, DOI: 10.20738/johb.30.1_8)
14.	Keiji Murakami, Tsuneko Ono, Darija Viducic, Yoko Somiya, Reiko Kariyama, Kenji Hori, Takashi Amoh, Katsuhiko Hirota, Hiromi Kumon, Matthew R. Parsek and Yoichiro Miyake : Role of psl Genes in Antibiotic Tolerance of Adherent Pseudomonas aeruginosa., Antimicrobial Agents and Chemotherapy, Vol.61, No.7, 2017. (Summary) Bacteria attached to a surface are generally more tolerant to antibiotics than their planktonic counterparts, even without the formation of a biofilm. The mechanism of antibiotic tolerance in biofilm communities is multifactorial, and the genetic background underlying this antibiotic tolerance has not yet been fully elucidated. Using transposon mutagenesis, we isolated a mutant with reduced tolerance to biapenem (relative to that of the wild type) from adherent cells. Sequencing analysis revealed a mutation in the pslL gene, which is part of the polysaccharide biosynthesis operon. The Pseudomonas aeruginosa PAO1 slBCD mutant demonstrated a 100-fold-lower survival rate during the exposure of planktonic and biofilm cells to biapenem; a similar phenotype was observed in a mouse infection model and in clinical strains. Transcriptional analysis of adherent cells revealed increased expression of both pslA and pelA, which are directly regulated by bis-(3',5')-cyclic dimeric GMP (c-di-GMP). Inactivation of wspF resulted in significantly increased tolerance to biapenem due to increased production of c-di-GMP. The loss of pslBCD in the spF mutant background abolished the biapenem-tolerant phenotype of the spF mutant, underscoring the importance of psl in biapenem tolerance. Overexpression of PA2133, which can catalyze the degradation of c-di-GMP, led to a significant reduction in biapenem tolerance in adherent cells, indicating that c-di-GMP is essential in mediating the tolerance effect. The effect of pslBCD on antibiotic tolerance was evident, with 50- and 200-fold-lower survival in the presence of ofloxacin and tobramycin, respectively. We speculate that the psl genes, which are activated by surface adherence through elevated intracellular c-di-GMP levels, confer tolerance to antimicrobials. (Link to Publication Site) ● Publication site (DOI): 10.1128/AAC.02587-16 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28438927 ● Search Scopus @ Elsevier (PMID): 28438927 ● Search Scopus @ Elsevier (DOI): 10.1128/AAC.02587-16 (DOI: 10.1128/AAC.02587-16, PubMed: 28438927)
15.	Kazuto Shiraishi, Noriko Saito-Tarashima, Yohsuke Igata, Keiji Murakami, Yasuko Okamoto, Yoichiro Miyake, Kazuhiro Furukawa and Noriaki Minakawa : Synthesis and evaluation of c-di-4'-thioAMP as an artificial ligand for c-di-AMP riboswitch, Bioorganic & Medicinal Chemistry, Vol.25, No.14, 3883-3889, 2017. (Summary) Cyclic-di-adenosine monophosphate (c-di-AMP) is a bacterial second messenger that binds to an RNA receptor called riboswitch and regulates its downstream genes involving cell wall metabolism, ion transport, and spore germination. Therefore, the c-di-AMP riboswitch can be a novel target of antibiotics. In this study, we synthesized c-di-4'-thioAMP (1), which possesses a sulfur atom instead of an oxygen atom in the furanose ring, as a candidate of a bioisoster for natural c-di-AMP. The resulting 1 bound to the c-di-AMP riboswitch with a micromolar affinity (34.8M), and the phosphodiesterase resistance of 1 was >12-times higher than that of c-di-AMP. Thus, 1 can be considered to be a stable ligand against a c-di-AMP riboswitch. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmc.2017.05.042 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28559057 ● Search Scopus @ Elsevier (PMID): 28559057 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmc.2017.05.042 (DOI: 10.1016/j.bmc.2017.05.042, PubMed: 28559057)
16.	Darija Viducic, Keiji Murakami, Takashi Amoh, Tsuneko Ono and Yoichiro Miyake : RpoN Promotes Pseudomonas aeruginosa Survival in the Presence of Tobramycin., Frontiers in Microbiology, Vol.8, 839, 2017. (Summary) Pseudomonas aeruginosa has developed diverse strategies to respond and adapt to antibiotic stress. Among the factors that modulate survival in the presence of antibiotics, alternative sigma factors play an important role. Here, we demonstrate that the alternative sigma factor RpoN ( (54)) promotes survival in the presence of tobramycin. The tobramycin-sensitive phenotype of logarithmic phase poN mutant cells is suppressed by the loss of the alternative sigma factor RpoS. Transcriptional analysis indicated that RpoN positively regulates the expression of RsmA, an RNA-binding protein, in the P. aeruginosa stationary growth phase in a nutrient-rich medium. The loss of RpoS led to the upregulation of gacA expression in the nutrient-limited medium-grown stationary phase cells. Conversely, in the logarithmic growth phase, the poS mutant demonstrated lower expression of gacA, underscoring a regulatory role of RpoS for GacA. Supplementation of tobramycin to stationary phase poN mutant cells grown in nutrient-rich medium resulted in decreased expression of gacA, relA, and rpoS without altering the expression of rsmA relative to wild-type PAO1. The observed downregulation of gacA and relA in the poN mutant in the presence of tobramycin could be reversed through the mutation of rpoS in the poN mutant background. The tobramycin-tolerant phenotype of the poN poS mutant logarithmic phase cells may be associated with the expression of relA, which remained unresponsive upon addition of tobramycin. The logarithmic phase poS and poN poS mutant cells demonstrated increased expression of gacA in response to tobramycin. Together, these results suggest that a complex regulatory interaction between RpoN, RpoS, the Gac/Rsm pathway, and RelA modulates the P. aeruginosa response to tobramycin. (Tokushima University Institutional Repository) ● Metadata: 114411 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2017.00839 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28553272 ● Search Scopus @ Elsevier (PMID): 28553272 ● Search Scopus @ Elsevier (DOI): 10.3389/fmicb.2017.00839 (Tokushima University Institutional Repository: 114411, DOI: 10.3389/fmicb.2017.00839, PubMed: 28553272)
17.	Natsumi Fujiwara, Keiji Murakami, Michiyasu Nakao, Munehisa Toguchi, Hiromichi Yumoto, Takashi Amoh, Katsuhiko Hirota, Takashi Matsuo, Shigeki Sano, Kazumi Ozaki and Yoichiro Miyake : Novel reuterin-related compounds suppress odour by periodontopathic bacteria, Oral Diseases, Vol.23, No.4, 492-497, 2017. (Summary) Halitosis is caused by volatile sulphur compounds including methyl mercaptan (CH3 SH) in the oral cavity and is a serious problem that limits interpersonal social communication. The aim of study was to evaluate the effects of reuterin-related compounds (RRCs) on halitosis-related periodontopathic bacteria in vitro. RRC-01, RRC-02 and RRC-03 (32 and 64 g ml(-1) ) in culture media containing Fusobacterium nucleatum JCM8523 and Porphyromonas gingivalis ATCC33277 were used. The effects of RRCs on CH3 SH production and detectable odour by F. nucleatum and P. gingivalis were examined by CH3 SH production assay and organoleptic test, respectively. The number of bacterial cells was also measured using an ATP assay. In P. gingivalis treated with RRCs, the expression of mgl gene, which is responsible for CH3 SH production, was examined by qRT-PCR. CH3 SH production and the score of detectable odour from F. nucleatum and P. gingivalis culture media containing RRCs were significantly lower than that without RRCs (P < 0.05). The expression of mgl gene in P. gingivalis was significantly downregulated by RRC-01 (P < 0.01), but not by RRC-02 or RRC-03. RRCs are potent oral care products for preventing halitosis via reducing CH3 SH production. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12638 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28083982 ● Summary page in Scopus @ Elsevier: 2-s2.0-85015084211 (DOI: 10.1111/odi.12638, PubMed: 28083982, Elsevier: Scopus)
18.	Keiji Murakami, Tsuneko Ono, Yasuki Noma, Issei Minase, Takashi Amoh, Yasuhiko Irie, Katsuhiko Hirota and Yoichiro Miyake : Explorative gene analysis of antibiotic tolerance-related genes in adherent and biofilm cells of Pseudomonas aeruginosa., Journal of Infection and Chemotherapy, Vol.23, No.5, 271-277, 2017. (Summary) Antibiotic tolerance has attracted worldwide attention, as it leads to chronic, refractory, and persistent infections that are difficult to control. Bacterial biofilms are well known to be more tolerant to antibiotics compared to planktonic bacteria. We previously revealed that adherent bacteria on a solid surface also exhibited tolerance to antibiotics before forming a biofilm. However, little is known about the mechanisms of antibiotic tolerance for adherent or biofilm cells. We investigated the mechanisms of antibiotic tolerance in the biofilm life cycle using adherent and biofilm cells, and evaluated the possibility that common mechanisms operate at each stage. We constructed transposon mutants of Pseudomonas aeruginosa PAO1 and screened for low-tolerant mutants with two different methods, using adherent cells and biofilm cells. Fourteen and nine mutants exhibiting low antibiotic tolerance were detected in the adherent cells and biofilm cells, and 14 and 7 candidate genes linked to this tolerance were identified by sequencing, respectively. Eight of the 14 genes related to the antibiotic tolerance of the adherent cells were involved in biofilm formation. Two of the seven genes related to the antibiotic tolerance of biofilm cells participated in the antibiotic tolerance of adherent cells. The antibiotic tolerance of adherent cells and biofilm formation appear to be under the same regulation mechanism to promote survival in the presence of antibiotics. Antibiotic tolerance shows a complex regulation mechanism at each stage of biofilm formation. (Keyword) Anti-Bacterial Agents / Biofilms / Humans / Microbial Sensitivity Tests / Mutation / Pseudomonas Infections / Pseudomonas aeruginosa (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jiac.2017.01.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28274550 ● Summary page in Scopus @ Elsevier: 2-s2.0-85014161002 (DOI: 10.1016/j.jiac.2017.01.004, PubMed: 28274550, Elsevier: Scopus)
19.	Darija Viducic, Keiji Murakami, Takashi Amoh, Tsuneko Ono and Yoichiro Miyake : Role of the interplay between quorum sensing regulator VqsR and the Pseudomonas quinolone signal in mediating carbapenem tolerance in Pseudomonas aeruginosa., Research in Microbiology, Vol.168, No.5, 450-460, 2017. (Summary) Pseudomonas aeruginosa coordinates its response to environmental conditions through activation of a quorum sensing (QS) system. In this study, we investigated the regulatory interaction between the QS transcriptional regulator VqsR and the Pseudomonas quinolone signal (PQS) through integration of sigma factor RpoS, and we addressed whether one of the pathways controlling carbapenem tolerance can be attributed to VqsR. We demonstrate that vqsR expression at the transcriptional level is regulated by pqsA, pqsR, and pqsE. Assessment of the transcriptional expression of vqsR, lasI, rhlI, and qscR in qsA and qsA poS mutants provided insight into pqsA- and rpoS-dependent regulation of vqsR and vqsR-controlled genes. Exogenously supplemented PQS reversed expression of vqsR and vqsR-controlled genes in the qsA mutant to wild-type levels, but failed to increase expression levels of lasI and qscR in the qsA poS mutant to levels observed in wild-type PAO1. The qsR mutant showed reduced survival when challenged with carbapenems compared to wild-type PAO1. Introduction of a pqsA mutation into the qsR mutant completely abolished its carbapenem-sensitive phenotype. We conclude that a regulatory link between PQS and vqsR exists, and that RpoS is important in their interaction. We also demonstrate that VqsR affects carbapenem tolerance. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.resmic.2017.02.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28263907 ● Search Scopus @ Elsevier (PMID): 28263907 ● Search Scopus @ Elsevier (DOI): 10.1016/j.resmic.2017.02.007 (DOI: 10.1016/j.resmic.2017.02.007, PubMed: 28263907)
20.	Keiji Murakami, Hiromichi Yumoto, Ayu Murakami, Takashi Amoh, Darija Viducic, Katsuhiko Hirota, Atsushi Tabata, Hideaki Nagamune, Hiroki Kourai, Takashi Matsuo and Yoichiro Miyake : Evaluation of the effectiveness of the potent bis-quaternary ammonium compound, 4,4'-( , -hexametylenedithio) bis (1-octylpyridinium bromide) (4DTBP-6,8) on Pseudomonas aeruginosa., Journal of Applied Microbiology, Vol.122, No.4, 893-899, 2017. (Summary) Quaternary ammonium compounds (QACs), including benzalkonium chloride (BAC) and cetylpyridinium chloride (CPC) are cationic surfactants and have been used widely as general disinfectants in the medical field due to their strong antibacterial effects and low cytotoxicity to human cells. 4,4'-( , -hexametylenedithio) bis (1-octylpyridinium bromide) (4DTBP-6,8) is one of the potent bis-QACs synthesized to improve the antimicrobial activities of mono-QACs such as BAC. This study aimed to assess the effectiveness of 4DTBP-6,8 against Pseudomonas aeruginosa, a prevalent hospital pathogen. The minimum inhibitory concentrations of 4DTBP-6,8, CPC and BAC against P. aeruginosa were measured. 4DTBP-6,8 exhibited strong antibacterial activity. We assessed the bactericidal effects of QACs against P. aeruginosa under certain conditions and their cytotoxicities in human epithelial cells using lactate dehydrogenase (LDH) release. 4DTBP-6,8 exerted excellent bactericidal effects against high concentrations of bacteria, biofilm cells and even in the presence of contaminated proteins. Cellular LDH was not released by the treatment with 4DTBP-6,8. 4DTBP-6,8 exhibited the strongest bactericidal activity against P. aeruginosa among the three QACs tested without any cytotoxicity. The potent bis-QAC, 4DTBP-6,8 has the potential to be an effective disinfectant in preventing hospital infections caused by P. aeruginosa. (Keyword) Anti-Bacterial Agents / Biofilms / Cell Line / Disinfectants / Humans / Niacinamide / Pseudomonas aeruginosa / Pyridinium Compounds (Link to Publication Site) ● Publication site (DOI): 10.1111/jam.13392 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28035713 ● Summary page in Scopus @ Elsevier: 2-s2.0-85013236835 (DOI: 10.1111/jam.13392, PubMed: 28035713, Elsevier: Scopus)
21.	Takashi Amoh, Keiji Murakami, Reiko Kariyama, Kenji Hori, Yasuhiko Irie, Darija Viducic, Katsuhiko Hirota, Jun Igarashi, Hiroaki Suga, Hiromi Kumon and Yoichiro Miyake : A Pseudomonas aeruginosa Quorum-Sensing autoinducer analog enhances the activity of antibiotics against resistant strains., The Journal of Medical Investigation : JMI, Vol.64, No.1.2, 101-109, 2017. (Summary) In this study, we have investigated the effects of the newly synthesized analog of Pseudomonas aeruginosa quorum-sensing autoinducer named AIA-1 (autoinducer analog) against antibiotic-resistant bacteria. In vitro susceptibility and killing assays for P. aeruginosa PAO1 prD mutant and clinical isolates were performed by using antibiotics and AIA-1. In an in vivo assay, a luminescent carbapenem-resistant strain derived from PAO1 prD was injected into neutropenic ICR mice and bioluminescence images were acquired after the treatment with antibiotics and AIA-1. Additionally, we investigated the effects of the combination use against carbapenem-resistant Enterobacteriaceae (CRE). Using killing assays in P. aeruginosa, the survival rates in the presence of antibiotics and AIA-1 significantly decreased in comparison with those with antibiotics alone. Furthermore, dual treatment of biapenem and AIA-1 was more effective than biapenem alone in a mouse infection model. AIA-1 did not change the MICs in P. aeruginosa, suggesting that AIA-1 acts on the mechanism of antibiotic tolerance. Conversely, the MICs of antibiotics decreased in the presence of AIA-1 in some CRE strains, indicating that AIA-1 may require additional mechanism to act on CRE. In conclusion, AIA-1 may be a potent drug for clinical treatment of infections caused by antibiotic-resistant bacteria. J. Med. Invest. 64: 101-109, February, 2017. (Tokushima University Institutional Repository) ● Metadata: 111094 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.101 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373605 ● Search Scopus @ Elsevier (PMID): 28373605 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.101 (Tokushima University Institutional Repository: 111094, DOI: 10.2152/jmi.64.101, PubMed: 28373605)
22.	Darija Viducic, Keiji Murakami, Takashi Amoh, Tsuneko Ono and Yoichiro Miyake : RpoN Modulates Carbapenem Tolerance in Pseudomonas aeruginosa through Pseudomonas Quinolone Signal and PqsE., Antimicrobial Agents and Chemotherapy, Vol.60, No.10, 5752-5764, 2016. (Summary) The ability of Pseudomonas aeruginosa to rapidly modulate its response to antibiotic stress and persist in the presence of antibiotics is closely associated with the process of cell-to-cell signaling. The alternative sigma factor RpoN ( (54)) is involved in the regulation of quorum sensing (QS) and plays an important role in the survival of stationary-phase cells in the presence of carbapenems. Here, we demonstrate that a poN mutant grown in nutrient-rich medium has increased expression of pqsA, pqsH, and pqsR throughout growth, resulting in the increased production of the Pseudomonas quinolone signal (PQS). The link between pqsA and its role in carbapenem tolerance was studied using a poN qsA mutant, in which the carbapenem-tolerant phenotype of the poN mutant was abolished. In addition, we demonstrate that another mechanism leading to carbapenem tolerance in the poN mutant is mediated through pqsE Exogenously supplied PQS abolished the biapenem-sensitive phenotype of the poN qsA mutant, and overexpression of pqsE failed to alter the susceptibility of the poN qsA mutant to biapenem. The mutations in the poN hlR mutant and the poN qsH mutant led to susceptibility to biapenem. Comparison of the changes in the expression of the genes involved in QS in wild-type PAO1 with their expression in the poN mutant and the poN mutant-derived strains demonstrated the regulatory effect of RpoN on the transcript levels of rhlR, vqsR, and rpoS The findings of this study demonstrate that RpoN negatively regulates the expression of PQS in nutrient-rich medium and provide evidence that RpoN interacts with pqsA, pqsE, pqsH, and rhlR in response to antibiotic stress. (Keyword) Bacterial Proteins / Carbapenems / Drug Resistance, Bacterial / Gene Expression Regulation, Bacterial / Microbial Sensitivity Tests / Mutation / Pseudomonas aeruginosa / Quinolones / quorum sensing / Sigma Factor / signal transduction / Trans-Activators (Link to Publication Site) ● Publication site (DOI): 10.1128/AAC.00260-16 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27431228 ● Summary page in Scopus @ Elsevier: 2-s2.0-84992643511 (DOI: 10.1128/AAC.00260-16, PubMed: 27431228, Elsevier: Scopus)
23.	Yasuko Sekita, Keiji Murakami, Hiromichi Yumoto, Takashi Amoh, Natsumi Fujiwara, Shohei Ogata, Takashi Matsuo, Yoichiro Miyake and Yoshiki Kashiwada : Preventive Effects of Houttuynia cordata Extract for Oral Infectious Diseases., BioMed Research International, Vol.2016, 2581876, 2016. (Summary) Houttuynia cordata (HC) (Saururaceae) has been used internally and externally as a traditional medicine and as an herbal tea for healthcare in Japan. Our recent survey showed that HC poultice (HCP) prepared from smothering fresh leaves of HC had been frequently used for the treatment of purulent skin diseases with high effectiveness. Our experimental study also demonstrated that ethanol extract of HCP (eHCP) has antibacterial, antibiofilm, and anti-inflammatory effects against S. aureus which caused purulent skin diseases. In this study, we focused on novel effects of HCP against oral infectious diseases, such as periodontal disease and dental caries. We determined the antimicrobial and antibiofilm effects of water solution of HCP ethanol extract (wHCP) against important oral pathogens and investigated its cytotoxicity and anti-inflammatory effects on human oral epithelial cells. wHCP had moderate antimicrobial effects against some oral microorganisms and profound antibiofilm effects against Fusobacterium nucleatum, Streptococcus mutans, and Candida albicans. In addition, wHCP had no cytotoxic effects and could inhibit interleukin-8 and CCL20 productions by Porphyromonas gingivalis lipopolysaccharide-stimulated human oral keratinocytes. Our findings suggested that wHCP may be clinically useful for preventing oral infectious diseases as a mouthwash for oral care. (Keyword) Anti-Bacterial Agents / bacteria / Biofilms / Cell Line / Cell Survival / Dental Caries / Houttuynia / Humans / Periodontal Diseases / Plant Extracts (Tokushima University Institutional Repository) ● Metadata: 112384 (Link to Publication Site) ● Publication site (DOI): 10.1155/2016/2581876 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27413739 ● Summary page in Scopus @ Elsevier: 2-s2.0-84978765486 (Tokushima University Institutional Repository: 112384, DOI: 10.1155/2016/2581876, PubMed: 27413739, Elsevier: Scopus)
24.	Yasuko Sekita, Keiji Murakami, Hiromichi Yumoto, Hiroyuki Mizuguchi, Takashi Amoh, Satoshi Ogino, Takashi Matsuo, Yoichiro Miyake, Hiroyuki Fukui and Yoshiki Kashiwada : Anti-bacterial and anti-inflammatory effects of ethanol extract from Houttuynia cordata poultice., Bioscience, Biotechnology, and Biochemistry, 2016. (Summary) Houttuynia cordata (HC) has been commonly used as many traditional remedies in local areas of Japan. Although many pharmacological activities of HC have been reported, the mechanism underlying the effect of HC remains unknown. We conducted the interview survey in Japan to verify how HC was actually used. The interview survey revealed that HC poultice (HCP) prepared from smothering fresh leaves of HC was most frequently used for the treatment of purulent skin diseases including furuncle and carbuncle with high effectiveness. Ethanol extract of HCP (eHCP) showed anti-bacterial effects against methicillin-resistant Staphylococcus aureus (MRSA), and showed an anti-biofilm activity against MRSA. eHCP showed dose-dependent inhibition of S. aureus lipoteichoic acid (LTA)-induced interleukin-8 and CCL20 production in human keratinocyte without any cytotoxicity. These results suggest that HCP is effective for skin abscess and its underlying mechanism might be the complicated multiple activities for both bacteria and host cells. (Link to Publication Site) ● Publication site (DOI): 10.1080/09168451.2016.1151339 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27023331 ● Search Scopus @ Elsevier (PMID): 27023331 ● Search Scopus @ Elsevier (DOI): 10.1080/09168451.2016.1151339 (DOI: 10.1080/09168451.2016.1151339, PubMed: 27023331)
25.	Hiromichi Yumoto, Katsuhiko Hirota, Kouji Hirao, Tsuyoshi Miyazaki, Nobuyuki Yamamoto, Koji Miyamoto, Keiji Murakami, Natsumi Fujiwara, Takashi Matsuo and Yoichiro Miyake : Anti-inflammatory and protective effects of 2-methacryloyloxyethyl phosphorylcholine polymer on oral epithelial cells., Journal of Biomedical Materials Research. Part A, Vol.103, No.2, 555-563, 2014. (Summary) Periodontitis is a chronic inflammatory disease initiated by a microbial biofilm formed in the periodontal pocket. Gingival epithelium plays important roles as the first physical barrier to bacterial invasion and in orchestrating the innate immune reaction via toll-like receptors (TLRs), which recognize various bacterial products, and maintaining its function. Newly developed oral care products to inhibit bacterial adherence, subsequent inflammatory reaction and protect the gingival epithelium are expected. We previously reported that 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymer coating decreased bacterial adhesion to human oral keratinocytes, RT-7, and mouth-rinsing with MPC-polymer inhibited the increase of oral bacteria. In this study, regarding the possibility of MPC-polymer application for preventing the adherence of periodontal pathogen, subsequent inflammatory reaction and protection of gingival epithelium, we examined the effects of MPC-polymer on the adherence of Porphyromonas gingivalis, major periodontitis-related pathogen, and TLR2 ligand to RT-7 and subsequent interleukin (IL)-8 production. MPC-polymer treatment significantly reduced P. gingivalis adherence by 44% and TLR2-mediated IL-8 production by blocking the binding of its specific-ligand in a concentration-dependent manner. Furthermore, MPC-polymer pretreatment protected RT-7 from injury by chemical irritants, cetylpyridinium chloride. These findings suggest that MPC-polymer is potentially useful for oral care to prevent oral infection and to maintain oral epithelial function. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2014. (Keyword) Anti-Inflammatory Agents / Bacteroidaceae Infections / Cell Line, Transformed / Epithelial Cells / Humans / Mouth / periodontitis / Phosphorylcholine / Polymethacrylic Acids / Porphyromonas gingivalis (Link to Publication Site) ● Publication site (DOI): 10.1002/jbm.a.35201 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24753309 ● Summary page in Scopus @ Elsevier: 2-s2.0-84924401882 (DOI: 10.1002/jbm.a.35201, PubMed: 24753309, Elsevier: Scopus)
26.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Effect of extracellular DNA on pyocyanin production from Pseudomonas aeruginosa, Bacterial Adherence & Biofilm, Vol.27, 45-47, 2014.
27.	狩山玲子, 堀賢司, 光畑律子, Keiji Murakami, 和田耕一郎, 石井亜矢乃, 渡辺豊彦, Yoichiro Miyake and 公文裕巳 : マウスを用いた緑膿菌性尿路バイオフィルム感染症モデルの作製, Bacterial Adherence & Biofilm, Vol.27, 67-71, 2014.
28.	B Sapaar, A Nur, Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, T Amoh, Takashi Matsuo, Tetsuo Ichikawa and Yoichiro Miyake : Effects of extracellular DNA from Candida albicans and pneumonia-related pathogens on Candida biofilm formation and hyphal transformation., Journal of Applied Microbiology, Vol.116, No.6, 1531-1542, 2014. (Summary) The aim of this study was to investigate the effects of genomic DNA purified from Candida albicans and pneumonia-related pathogens, Pseudomonas aeruginosa and Staphylococcus aureus, on in vitro biofilm formation and morphological change of 3 Candida species (C. albicans, C. glabrata, and C. tropicalis). Biofilm formation was evaluated by the crystal violet assay and colony-forming unit counts. Morphological characteristics of biofilms were evaluated by scanning electron microscopy and fluorescence microscopy. Addition of DNA at a low concentration (<1·0 μg ml(-1)) significantly increased biofilm mass of all three Candida species. In contrast, the addition of DNA at a high concentration (10 μg ml(-1)) decreased the biofilm mass. Interestingly, the formation of hyphae in a dense network of yeast cells was observed in C. albicans biofilms exposed to a low concentration of DNA (<1·0 μg ml(-1)). These findings demonstrated that extracellular DNA (eDNA) plays a crucial role in Candida biofilm formation and suggested that eDNA may induce the morphological transition from yeast to hyphal growth form during C. albicans biofilm development. A novel therapy targeting eDNA may be applicable for Candida infection to decrease biofilm formation and hyphal formation. (Link to Publication Site) ● Publication site (DOI): 10.1111/jam.12483 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24661775 ● Summary page in Scopus @ Elsevier: 2-s2.0-84900806168 (DOI: 10.1111/jam.12483, PubMed: 24661775, Elsevier: Scopus)
29.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : 付着及びバイオフィルム形成緑膿菌の抗菌薬抵抗性関連遺伝子の探索, Bacterial Adherence & Biofilm, Vol.26, 237-238, 2013.
30.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Role of Extracellular DNA and DNA-binding protein in biofilm formation of Streptococcus intermeius, Bacterial Adherence & Biofilm, Vol.26, 25-29, 2013.
31.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, D Liu, Kanako Takahashi, Keiji Murakami, Takashi Matsuo, R Shu and Yoichiro Miyake : Effects of extracellular DNA and DNA-binding protein on the development of a Streptococcus intermedius biofilm., Journal of Applied Microbiology, Vol.115, No.1, 260-270, 2013. (Summary) The aim of this study was to clarify the effects of homologous and heterologous extracellular DNAs (eDNAs) and histone-like DNA-binding protein (HLP) on Streptococcus intermedius biofilm development and rigidity. Formed biofilm mass was measured with 0·1% crystal violet staining method and observed with a scanning electron microscope. The localizations of eDNA and extracellular HLP (eHLP) in formed biofilm were detected by staining with 7-hydoxyl-9H-(1,3-dichloro-9,9-dimethylacridin-2-one) and anti-HLP antibody without fixation, respectively. DNase I treatment (200 U ml(-1) ) markedly decreased biofilm formation and cell density in biofilms. Colocalization of eHLP and eDNA in biofilm was confirmed. The addition of eDNA (up to 1 μg ml(-1) ) purified from Strep. intermedius, other Gram-positive bacteria, Gram-negative bacteria, or human KB cells into the Strep. intermedius culture increased the biofilm mass of all tested strains of Strep. intermedius, wild-type, HLP-downregulated strain and control strains. In contrast, the addition of eDNA (>1 μg ml(-1) ) decreased the biofilm mass of all Strep. intermedius strains. These findings demonstrated that eDNA and eHLP play crucial roles in biofilm development and its rigidity. eDNA- and HLP-targeting strategies may be applicable to novel treatments for bacterial biofilm-related infectious diseases. (Keyword) Biofilms / Cell Line, Tumor / DNA / DNA-Binding Proteins / Deoxyribonuclease I / Humans / Streptococcus intermedius (Tokushima University Institutional Repository) ● Metadata: 106279 (Link to Publication Site) ● Publication site (DOI): 10.1111/jam.12202 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23551549 ● Summary page in Scopus @ Elsevier: 2-s2.0-84879085342 (Tokushima University Institutional Repository: 106279, DOI: 10.1111/jam.12202, PubMed: 23551549, Elsevier: Scopus)
32.	Morten T. Rybtke, Bradley R. Borlee, Keiji Murakami, Yasuhiko Irie, Morten Hentzer, Thomas E. Nielsen, Michael Givskov, Matthew R. Parsek and Tim Tolker-Nielsen : Fluorescence-based reporter for gauging cyclic di-GMP levels in Pseudomonas aeruginosa., Applied and Environmental Microbiology, Vol.78, No.15, 5060-5069, 2012. (Summary) The increased tolerance toward the host immune system and antibiotics displayed by biofilm-forming Pseudomonas aeruginosa and other bacteria in chronic infections such as cystic fibrosis bronchopneumonia is of major concern. Targeting of biofilm formation is believed to be a key aspect in the development of novel antipathogenic drugs that can augment the effect of classic antibiotics by decreasing antimicrobial tolerance. The second messenger cyclic di-GMP is a positive regulator of biofilm formation, and cyclic di-GMP signaling is now regarded as a potential target for the development of antipathogenic compounds. Here we describe the development of fluorescent monitors that can gauge the cellular level of cyclic di-GMP in P. aeruginosa. We have created cyclic di-GMP level reporters by transcriptionally fusing the cyclic di-GMP-responsive cdrA promoter to genes encoding green fluorescent protein. We show that the reporter constructs give a fluorescent readout of the intracellular level of cyclic di-GMP in P. aeruginosa strains with different levels of cyclic di-GMP. Furthermore, we show that the reporters are able to detect increased turnover of cyclic di-GMP mediated by treatment of P. aeruginosa with the phosphodiesterase inducer nitric oxide. Considering that biofilm formation is a necessity for the subsequent development of a chronic infection and therefore a pathogenicity trait, the reporters display a significant potential for use in the identification of novel antipathogenic compounds targeting cyclic di-GMP signaling, as well as for use in research aiming at understanding the biofilm biology of P. aeruginosa. (Keyword) Adhesins, Bacterial / Biofilms / Cyclic GMP / Fluorescence / Genes, Reporter / Green Fluorescent Proteins / Plasmids / Promoter Regions, Genetic / Pseudomonas aeruginosa (Link to Publication Site) ● Publication site (DOI): 10.1128/AEM.00414-12 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22582064 ● Search Scopus @ Elsevier (PMID): 22582064 ● Search Scopus @ Elsevier (DOI): 10.1128/AEM.00414-12 (DOI: 10.1128/AEM.00414-12, PubMed: 22582064)
33.	Claudine Baraquet, Keiji Murakami, Matthew R. Parsek and Caroline S. Harwood : The FleQ protein from Pseudomonas aeruginosa functions as both a repressor and an activator to control gene expression from the pel operon promoter in response to c-di-GMP., Nucleic Acids Research, Vol.40, No.15, 7207-7218, 2012. (Summary) Bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP) modulates the transition between planktonic and biofilm life styles. In response to c-di-GMP, the enhancer binding protein FleQ from Pseudomonas aeruginosa derepresses the expression of Pel exopolysaccharide genes required for biofilm formation when a second protein, FleN is present. A model is that binding of c-di-GMP to FleQ induces its dissociation from the pelA promoter allowing RNA polymerase to access this site. To test this, we analyzed pelA DNA footprinting patterns with various combinations of FleQ, FleN and c-di-GMP, coupled to in vivo promoter activities. FleQ binds to two sites called box 1 and 2. FleN binds to FleQ bound at these sites causing the intervening DNA to bend. Binding of c-di-GMP to FleQ relieves the DNA distortion but FleQ remains bound to the two sites. Analysis of wild type and mutated versions of pelA-lacZ transcriptional fusions suggests that FleQ represses gene expression from box 2 and activates gene expression in response to c-di-GMP from box 1. The role of c-di-GMP is thus to convert FleQ from a repressor to an activator. The mechanism of action of FleQ is distinct from that of other bacterial transcription factors that both activate and repress gene expression from a single promoter. (Keyword) Adenosine Diphosphate / Adenosine Triphosphate / Bacterial Proteins / Binding Sites / Cyclic GMP / DNA, Bacterial / Gene Expression Regulation, Bacterial / Operon / Promoter Regions, Genetic / Pseudomonas aeruginosa / Repressor Proteins / Trans-Activators (Link to Publication Site) ● Publication site (DOI): 10.1093/nar/gks384 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22581773 ● Search Scopus @ Elsevier (PMID): 22581773 ● Search Scopus @ Elsevier (DOI): 10.1093/nar/gks384 (DOI: 10.1093/nar/gks384, PubMed: 22581773)
34.	Katsuhiko Hirota, Hiromichi Yumoto, K Miyamoto, N Yamamoto, Keiji Murakami, Yumi Hoshimo, Takashi Matsuo and Yoichiro Miyake : MPC-Polymer Reduces Adherence and Biofilm Formation by Oral Bacteria., Journal of Dental Research, Vol.90, No.7, 900-905, 2011. (Summary) Oral biofilms such as dental plaque cause dental caries and periodontitis, as well as aspiration pneumonia and infectious endocarditis by translocation. Hence, the suppression of oral biofilm formation is an issue of considerable importance. Mechanical removal, disinfectants, inhibition of polysaccharide formation, and artificial sugar have been used for the reduction of oral biofilm. From the viewpoint of the inhibition of bacterial adherence, we investigated whether aqueous biocompatible 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymer can reduce streptococcal colonization and biofilm formation. We examined the effects of MPC-polymer on streptococcal adherence to saliva-coated hydroxyapatite and oral epithelial cells, and the adherence of Fusobacterium nucleatum to streptococcal biofilm. MPC-polymer application markedly inhibited both the adherence and biofilm formation of Streptococcus mutans on saliva-coated hydroxyapatite and streptococcal adherence to oral epithelial cells, and reduced the adherence of F. nucleatum to streptococcal biofilms. A small-scale clinical trial revealed that mouthrinsing with MPC-polymer inhibited the increase of oral bacterial numbers, especially of S. mutans. These findings suggest that MPC-polymer is a potent inhibitor of bacterial adherence and biofilm development, and may be useful to prevent dental-plaque-related diseases. (UMIN Clinical Trial Registry UMIN000003471). Abbreviations: QOL, quality of life; MPC, 2-methacryloyloxyethyl phosphorylcholine; BHI, brain-heart infusion broth; PBS, phosphate-buffered saline; SEM, scanning electron microscopy; CFU, colony-forming unit. (Link to Publication Site) ● Publication site (DOI): 10.1177/0022034511402996 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21447697 ● Summary page in Scopus @ Elsevier: 2-s2.0-84884211413 (DOI: 10.1177/0022034511402996, PubMed: 21447697, Elsevier: Scopus)
35.	M Kelly Colvin, D Vernita Gordon, Keiji Murakami, R Bradley Borlee, J Daniel Wozniak, L Gerard C Wong and R Matthew Parsek : The pel polysaccharide can serve a structural and protective role in the biofilm matrix of Pseudomonas aeruginosa., PLoS Pathogens, Vol.7, No.1, e1001264, 2011. (Summary) Bacterial extracellular polysaccharides are a key constituent of the extracellular matrix material of biofilms. Pseudomonas aeruginosa is a model organism for biofilm studies and produces three extracellular polysaccharides that have been implicated in biofilm development, alginate, Psl and Pel. Significant work has been conducted on the roles of alginate and Psl in biofilm development, however we know little regarding Pel. In this study, we demonstrate that Pel can serve two functions in biofilms. Using a novel assay involving optical tweezers, we demonstrate that Pel is crucial for maintaining cell-to-cell interactions in a PA14 biofilm, serving as a primary structural scaffold for the community. Deletion of pelB resulted in a severe biofilm deficiency. Interestingly, this effect is strain-specific. Loss of Pel production in the laboratory strain PAO1 resulted in no difference in attachment or biofilm development; instead Psl proved to be the primary structural polysaccharide for biofilm maturity. Furthermore, we demonstrate that Pel plays a second role by enhancing resistance to aminoglycoside antibiotics. This protection occurs only in biofilm populations. We show that expression of the pel gene cluster and PelF protein levels are enhanced during biofilm growth compared to liquid cultures. Thus, we propose that Pel is capable of playing both a structural and a protective role in P. aeruginosa biofilms. (Keyword) Alginates / Anti-Bacterial Agents / Bacterial Adhesion / Bacterial Proteins / Biofilms / Extracellular Matrix / Gene Expression Regulation, Bacterial / Microbial Sensitivity Tests / Microbial Viability / Polysaccharides, Bacterial / Pseudomonas aeruginosa / Tobramycin (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.ppat.1001264 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21298031 ● Search Scopus @ Elsevier (PMID): 21298031 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.ppat.1001264 (DOI: 10.1371/journal.ppat.1001264, PubMed: 21298031)
36.	Heni Susilowati, Hirohiko Okamura, Katsuhiko Hirota, Masayuki Shono, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji and Yoichiro Miyake : Intermedilysin induces EGR-1 expression through calcineurin/NFAT pathway in human cholangiocellular carcinoma cells., Biochemical and Biophysical Research Communications, Vol.404, No.1, 57-61, 2011. (Summary) (Intermedilysin (ILY) is a cholesterol-dependent cytolysin produced by Streptococcus intermedius, which is associated with human brain and liver abscesses. Although intrahepatic bile duct cells play a valuable role in the pathogenesis of liver abscess, the molecular mechanism of ILY-treated intrahepatic bile duct cells remains unknown. In this study, we report that ILY induced a nuclear accumulation of intracellular calcium ([Ca(2+)]i) in human cholangiocellular cells HuCCT1. We also demonstrate that 10 ng/ml ILY induced NFAT1 dephosphorylation and its nuclear translocation in HuCCT1 cells. In contrast to the result that ILY induced NF-B translocation in human hepatic HepG2 cells, ILY did not affect NF-B localization in HuCCT1 cells. Dephosphorylation and nuclear translocation of NFAT1 caused by ILY were prevented by [Ca(2+)]i calcium chelator, BAPTA/AM, and calcineurin inhibitors, cyclosporine A and tacrolimus. ILY induced early growth response-1 (EGR-1) expression and it was inhibited by the pre-treatment with cyclosporine A, indicating that the calcineurin/NFAT pathway was involved in EGR-1 expression in response to ILY. ILY-induced calcineurin/NFAT1 activation and sequential EGR-1 expression might be related to the pathogenesis of S. intermedius in human bile duct cells.) (Keyword) Bacteriocins / Bile Ducts, Intrahepatic / Calcineurin / calcium / Cell Line, Tumor / Cell Nucleus / Early Growth Response Protein 1 / Humans / NFATC Transcription Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2010.11.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21094139 ● Summary page in Scopus @ Elsevier: 2-s2.0-78650872240 (DOI: 10.1016/j.bbrc.2010.11.057, PubMed: 21094139, Elsevier: Scopus)
37.	Bradley R. Borlee, Aaron D. Goldman, Keiji Murakami, Ram Samudrala, Daniel J. Wozniak and Matthew R. Parsek : Pseudomonas aeruginosa uses a cyclic-di-GMP-regulated adhesin to reinforce the biofilm extracellular matrix., Molecular Microbiology, Vol.75, No.4, 827-842, 2010. (Summary) Pseudomonas aeruginosa, the principal pathogen of cystic fibrosis patients, forms antibiotic-resistant biofilms promoting chronic colonization of the airways. The extracellular (EPS) matrix is a crucial component of biofilms that provides the community multiple benefits. Recent work suggests that the secondary messenger, cyclic-di-GMP, promotes biofilm formation. An analysis of factors specifically expressed in P. aeruginosa under conditions of elevated c-di-GMP, revealed functions involved in the production and maintenance of the biofilm extracellular matrix. We have characterized one of these components, encoded by the PA4625 gene, as a putative adhesin and designated it cdrA. CdrA shares structural similarities to extracellular adhesins that belong to two-partner secretion systems. The cdrA gene is in a two gene operon that also encodes a putative outer membrane transporter, CdrB. The cdrA gene encodes a 220 KDa protein that is predicted to be rod-shaped protein harbouring a beta-helix structural motif. Western analysis indicates that the CdrA is produced as a 220 kDa proprotein and processed to 150 kDa before secretion into the extracellular medium. We demonstrated that cdrAB expression is minimal in liquid culture, but is elevated in biofilm cultures. CdrAB expression was found to promote biofilm formation and auto-aggregation in liquid culture. Aggregation mediated by CdrA is dependent on the Psl polysaccharide and can be disrupted by adding mannose, a key structural component of Psl. Immunoprecipitation of Psl present in culture supernatants resulted in co-immunoprecipitation of CdrA, providing additional evidence that CdrA directly binds to Psl. A mutation in cdrA caused a decrease in biofilm biomass and resulted in the formation of biofilms exhibiting decreased structural integrity. Psl-specific lectin staining suggests that CdrA either cross-links Psl polysaccharide polymers and/or tethers Psl to the cells, resulting in increased biofilm structural stability. Thus, this study identifies a key protein structural component of the P. aeruginosa EPS matrix. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2958.2009.06991.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20088866 ● Search Scopus @ Elsevier (PMID): 20088866 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2958.2009.06991.x (DOI: 10.1111/j.1365-2958.2009.06991.x, PubMed: 20088866)
38.	Yuka Yoshijima, Keiji Murakami, Shizuo Kayama, Dali Liu, Katsuhiko Hirota, Tetsuo Ichikawa and Yoichiro Miyake : Effect of substrate surface hydrophobicity on the adherence of yeast and hyphal Candida, Mycoses, Vol.53, No.3, 221-226, 2009. (Summary) A biofilm composed of various microorganisms including Candida is found on denture surfaces and is likely to be involved in the etiology of denture-induced stomatitis. The purpose of this study was to examine the role of hydrophobic interactions in candidal adherence to acrylic surfaces, particularly that of the hyphal form of Candida albicans. Candida clinical isolates were used. Acrylic plates coated with carrageenan and hydrocolloid (Hitachi chemical, Tokyo, Japan) were used as a hydrophilic substratum. A microbial suspension was placed on each acrylic plate and incubated. All plates were washed in phosphate-buffered saline containing CaCl(2) and MgCl(2) [PBS (+)] and cells still adhering to the acrylic surface were collected by 0.25% trypsin treatment. Cell-surface hydrophobicity was estimated using a modification of the technique used to measure adherence to hydrocarbons. When the acrylic plates were coated with hydrophilic materials, the adherence of hydrophobic clinical isolates of Candida and the hydrophobic hyphal C. albicans decreased, whereas the adherence of non-hydrophobic Candida was not affected or increased. We suggest that hydrophilic coating of denture surfaces could be a potent method for reduction of the adherence of relatively hydrophobic fungal cells, particularly hyphal C. albicans, which causes denture stomatitis and related infections. (Keyword) Candida albicans / Candidiasis / Carrageenan / Cell Adhesion / Colloids / Hydrophobic and Hydrophilic Interactions / Hyphae / Yeasts (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1439-0507.2009.01694.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19671080 ● Search Scopus @ Elsevier (PMID): 19671080 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1439-0507.2009.01694.x (DOI: 10.1111/j.1439-0507.2009.01694.x, PubMed: 19671080)
39.	Shizuo Kayama, Keiji Murakami, Tsuneko Ono, Makiko Ushimaru, Akitake Yamamoto, Katsuhiko Hirota and Yoichiro Miyake : The role of rpoS gene and quorum-sensing system in ofloxacin tolerance in Pseudomonas aeruginosa, FEMS Microbiology Letters, Vol.298, No.2, 184-192, 2009. (Summary) The basis of the bactericidal action of antibiotics and the mechanisms of antibiotic tolerance are largely unknown. To elucidate one of the mechanisms of antibiotic tolerance, the present study investigated the role of Pseudomonas aeruginosa quorum sensing (QS) and the rpoS gene in antibiotic tolerance. The survival rates of the lasR and lasI mutants were observed to be lower than that of the parental strain in time-dependent killing studies with 8 microg mL(-1) ofloxacin, but the survival rates of the rhlR and rhlI mutants were not different from that of the parental strain. Moreover, a lasR-overexpressing strain was more tolerant to ofloxacin than the parental strain, but this was not the case for an rhlR-overexpressing strain. The mRNA expression levels of lasR, lasI, and rpoS in the wild-type strain in the presence of bactericidal concentration of ofloxacin were lower than that in the absence of ofloxacin. In addition, the significant loss of antibiotic tolerance in the lasR mutant was recovered by the overexpression of rpoS. These results suggest that the Las QS system in P. aeruginosa is involved in the development of ofloxacin tolerance, and the tolerance induced by the Las-system is regulated by rpoS gene. (Keyword) Anti-Bacterial Agents / Bacterial Proteins / Gene Deletion / Gene Expression Profiling / Ligases / Microbial Viability / Ofloxacin / Pseudomonas aeruginosa / quorum sensing / Sigma Factor / Time Factors / Trans-Activators / Transcription Factors (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1574-6968.2009.01717.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19645822 ● Summary page in Scopus @ Elsevier: 2-s2.0-68949207968 (DOI: 10.1111/j.1574-6968.2009.01717.x, PubMed: 19645822, Elsevier: Scopus)
40.	Liu Dali, Hiromichi Yumoto, Keiji Murakami, Katsuhiko Hirota, Shizuo Kayama, Taniguchi Tomonori, Yamamoto Akitake, Tsuneko Ono, Takashi Matsuo and Yoichiro Miyake : Heterologous expression of a histone-like protein from Streptococcus intermedius in Escherichia coli alters the nucleoid structure and inhibits the growth of E. coli, FEMS Microbiology Letters, Vol.288, No.1, 68-75, 2008. (Summary) Escherichia coli failed to survive after transformation with a Streptococcus intermedius histone-like protein gene (Si-hlp) and its promoter-harbored plasmid. The promoter function of Si-hlp in E. coli was determined using enhanced green fluorescence protein (egfp) gene as a reporter. The inhibitory effect of Si-HLP on E. coli viability was verified by a tetracycline-inducible gene expression system. Further study suggested that Si-HLP may alter the bacterial nucleoid structure, leading to the growth inhibition of E. coli. (Keyword) Bacterial Proteins / Cell Nucleolus / Cloning, Molecular / DNA, Bacterial / DNA, Superhelical / Escherichia coli / gene expression / Histones / Streptococcus intermedius (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1574-6968.2008.01327.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18761672 ● Summary page in Scopus @ Elsevier: 2-s2.0-52649125775 (DOI: 10.1111/j.1574-6968.2008.01327.x, PubMed: 18761672, Elsevier: Scopus)
41.	Liu Dali, Hiromichi Yumoto, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono, Hideaki Nagamune, Shizuo Kayama, Takashi Matsuo and Yoichiro Miyake : The essentiality and involvement of Streptococcus intermedius histone-like DNA-binding protein in bacterial viability and normal growth, Molecular Microbiology, Vol.68, No.5, 1268-1282, 2008. (Summary) Streptococcus intermedius histone-like DNA-binding protein (Si-HLP) is a homodimeric protein and, conserved with Escherichia coli HU, a well-documented nucleoid-associated protein (NAP). In E. coli, HU plays important roles as both structural and regulatory factors, but it is not essential for E. coli viability. Streptococcal HLP has been found to bind host cells and induce cytokine production, but its physiological role remains poorly defined. In the present study, using gene insertion knockout and tetracycline-regulated antisense RNA expression techniques, we determined whether Si-HLP is essential for bacterial viability and normal growth in S. intermedius. The Si-HLP-downregulated S. intermedius strain showed alterations in its morphology and surface properties. Downregulation of Si-HLP led to an expanded nucleoid to fill the intracellular space. Transcription levels of several genes, including virulence-associated factors, were found to be activated or repressed in the antisense Si-hlp RNA-expressing strain by real-time PCR and reverse-transcription PCR. Collectively, these data suggest that Si-HLP serves as an essential NAP governing the nucleoid architecture and controlling the gene transcription profile in S. intermedius. (Keyword) Bacterial Proteins / DNA-Binding Proteins / Escherichia coli Proteins / Gene Expression Regulation, Bacterial / Histones / Microbial Viability / Streptococcus intermedius / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2958.2008.06232.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18410499 ● Summary page in Scopus @ Elsevier: 2-s2.0-43749117518 (DOI: 10.1111/j.1365-2958.2008.06232.x, PubMed: 18410499, Elsevier: Scopus)
42.	Dali Liu, Hiromichi Yumoto, Katsuhiko Hirota, Keiji Murakami, Kanako Takahashi, Kouji Hirao, Takashi Matsuo, Kazuto Ohkura, Hideaki Nagamune and Yoichiro Miyake : Histone-like DNA binding protein of Streptococcus intermedius induces the expression of pro-inflammatory cytokines in human monocytes via action of ERK1/2 and JNK pathways, Cellular Microbiology, Vol.10, No.1, 262-276, 2008. (Summary) Streptococcus intermedius is a commensal associated with serious, deep-seated purulent infections in major organs, such as the brain and liver. Histone-like DNA binding protein (HLP) is an accessory architectural protein in a variety of bacterial cellular processes. In this study, we investigated the mechanisms of pro-inflammatory cytokine inductions in THP-1 cells by stimulation with recombinant HLP of S. intermedius (rSi-HLP). rSi-HLP stimulation-induced production of pro-inflammatory cytokines (IL-8, IL-1 beta and TNF-alpha) occurred in a time- and dose-dependent manner. In contrast with the heat-stable activity of DNA binding, the induction activity of rSi-HLP was heat-unstable. In subsequent studies, rSi-HLP acted cooperatively with lipoteichoic acid, the synthetic Toll-like receptor 2 agonist, Pam3CSK4, and the cytosolic nucleotide binding oligomerization domain 2 receptor agonist, muramyldipeptide. Furthermore, Western blot and blocking assays with specific inhibitors showed that rSi-HLP stimulation induced the activation of cell signal transduction pathways, extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK). In addition to its physiological role in bacterial growth through DNA binding, these results indicate that Si-HLP can trigger a cascade of events that induce pro-inflammatory responses via ERK1/2 and JNK signal pathways, and suggest that bacterial HLP may contribute to the activation of host innate immunity during bacterial infection. (Keyword) Acetylmuramyl-Alanyl-Isoglutamine / Bacterial Proteins / Cell Line / Cytokines / DNA, Bacterial / DNA-Binding Proteins / Hot Temperature / Humans / JNK Mitogen-Activated Protein Kinases / Lipopolysaccharides / Mitogen-Activated Protein Kinase 3 / Molecular Sequence Data / Monocytes / Recombinant Proteins / Sequence Analysis, DNA / Signal Transduction / Streptococcus intermedius / Teichoic Acids / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1462-5822.2007.01040.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17883418 ● Search Scopus @ Elsevier (PMID): 17883418 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1462-5822.2007.01040.x (DOI: 10.1111/j.1462-5822.2007.01040.x, PubMed: 17883418)
43.	Darija Viducic, Tsuneko Ono, Keiji Murakami, Katakami Mikiko, Susilowati Heni and Yoichiro Miyake : rpoN gene of Pseudomonas aeruginosa alters Its susceptibility to quinolones and cabapenems, Antimicrobial Agents and Chemotherapy, Vol.51, No.4, 1455-1462, 2007. (Summary) The alternative sigma factor sigma54 has been implicated in diverse functions within the cells. In this study, we have constructed an rpoN mutant of Pseudomonas aeruginosa and investigated its importance as a target for antimicrobial agents, such as quinolones and carbapenems. The stationary-phase cells of the rpoN mutant displayed a survival rate approximately 15 times higher than that of the wild-type cells in the presence of quinolones and carbapenems. The stationary phase led to substantial production of pyoverdine by the P. aeruginosa rpoN mutant. Pyoverdine synthesis correlated with decreased susceptibility to antimicrobial agents. Quantitative real-time PCR revealed that stationary-phase cells of the rpoN mutant grown without an antimicrobial agent had approximately 4- to 140- and 2- to 14-fold-higher levels of transcripts of the pvdS and vqsR genes, respectively, than the wild-type strain. In the presence of an antimicrobial agent, levels of pvdS and vqsR transcripts were elevated 400- and 5-fold, respectively, in comparison to the wild-type levels. Flow cytometry assays using a green fluorescent protein reporter demonstrated increased expression of the vqsR gene in the rpoN mutant throughout growth. A pvdS mutant of P. aeruginosa, deficient in pyoverdine production, was shown to be susceptible to biapenem. These findings suggest that rpoN is involved in tolerance to antimicrobial agents in P. aeruginosa and that its tolerant effect is partly dependent on increased pyoverdine production and vqsR gene expression. (Keyword) Carbapenems / Gene Expression Regulation, Bacterial / Genes, Bacterial / Promoter Regions, Genetic / Pseudomonas aeruginosa / Quinolones / RNA Polymerase Sigma 54 / Transcription, Genetic / Virulence (Link to Publication Site) ● Publication site (DOI): 10.1128/AAC.00348-06 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17261620 ● Summary page in Scopus @ Elsevier: 2-s2.0-34247154268 (DOI: 10.1128/AAC.00348-06, PubMed: 17261620, Elsevier: Scopus)
44.	Darija Viducic, Tsuneko Ono, Keiji Murakami, Susilowati Heni, Shizuo Kayama, Katsuhiko Hirota and Yoichiro Miyake : Functional Analysis of spoT, relA and dksA Genes on Quinolone Tolerance in Pseudomonas aeruginosa under Nongrowing Condition, Microbiology and Immunology, Vol.50, No.4, 349-357, 2006. (Summary) To assess the contribution of ppGpp in antibiotic tolerance to quinolone in Pseudomonas aeruginosa, knockout mutants of the genes involved or linked with the stringent response, such as relA, spoT and dksA, were constructed and investigated for their antibiotic susceptibility to quinolones. The survival of the dksA and spoT mutants in the presence of 8 microg/ml of ofloxacin and 1 microg/ml of ciprofloxacin were shown to be approximately 20-180 and 10-40 times respectively, higher than the same for the wild type strain. The intracellular levels of ppGpp determined with high performance liquid chromatography (HPLC) demonstrated that spoT and dksA mutants possess higher basal levels of ppGpp. The data suggest that elevated basal levels of ppGpp may be responsible for rendering these mutants tolerant to quinolones and expand the importance of ppGpp as an antimicrobial target in P. aeruginosa. (Keyword) Ciprofloxacin / Drug Resistance / Guanosine Tetraphosphate / Microbial Sensitivity Tests / Ofloxacin / Pseudomonas aeruginosa / Quinolones (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16625057 ● Search Scopus @ Elsevier (PMID): 16625057 (PubMed: 16625057)
45.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae, Keiji Murakami, Yoichiro Miyake and Takashi Matsuo : CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease, Clinical and Experimental Immunology, Vol.141, No.3, 467-474, 2005. (Summary) CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response. (Keyword) CXCL12 / CXCR4 / fibroblast / periodontal disease / Porphyromonas gingivalis (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2005.02852.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16045736 ● Search Scopus @ Elsevier (PMID): 16045736 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02852.x (DOI: 10.1111/j.1365-2249.2005.02852.x, PubMed: 16045736)
46.	Katsuhiko Hirota, Keiji Murakami, Ken Nemoto and Yoichiro Miyake : Coating of a surface with 2-methacryloyloxyethyl phosphorylcholine (MPC) co-polymer significantly reduces retention of human pathogenic microorganisms, FEMS Microbiology Letters, Vol.248, No.1, 37-45, 2005. (Summary) The present study compares the retention of four species that are often isolated in association with biomedical device-related infections - Staphylococcus aureus, Streptococcus mutans, Pseudomonas aeruginosa, and Candida albicans - to three different surfaces. All four bacterial species were found to bind significantly less well to MPC-coated surfaces than to non-coated surfaces. We attribute this effect to the "superhydrophilicity" of MPC-coated surfaces, whereas hydrophobic surfaces are well known to reduce bacterial retention and thus to inhibit a crucial step in the formation of bacterial biofilms that lead to biomedical device-related infections and complications. (Keyword) 2-Methacryloyloxyethyl phosphorylcholine / Superhydrophilicity / Hydrophobic / Microbial retention (Link to Publication Site) ● Publication site (DOI): 10.1016/j.femsle.2005.05.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15953697 ● Summary page in Scopus @ Elsevier: 2-s2.0-20444482366 (DOI: 10.1016/j.femsle.2005.05.019, PubMed: 15953697, Elsevier: Scopus)
47.	Keiji Murakami, Tsuneko Ono, Darija Viducic, Shizuo Kayama, Makiko Mori, Katsuhiko Hirota, Ken Nemoto and Yoichiro Miyake : Role for rpoS gene of Pseudomonas aeruginosa in antibiotic tolerance, FEMS Microbiology Letters, Vol.242, No.1, 161-167, 2005. (Summary) The alternative sigma factor, RpoS has been described as a central regulator of many stationary phase-inducible genes and a master stress-response regulator under various stress conditions. We constructed an rpoS mutant in Pseudomonas aeruginosa and investigated the role of rpoS gene in antibiotic tolerance. The survival of the rpoS mutant cells in stationary phase was approximately 70 times lower when compared with that of the parental strain at 37 degrees C for 2 h after the addition of biapenem. For imipenem, the survival was approximately 40 times lower. Heat stress promoted an increase in the survival of the parental strain to biapenem, but the same was not found to be the case for the rpoS mutant. Our results indicate that rpoS gene is involved in tolerance to antibiotics in P. aeruginosa during the stationary phase and heat stress. However, under osmotic stress, tolerance to biapenem was not dependent on the rpoS gene. (Keyword) Pseudomonas aeruginosa / Tolerance / rpoS gene (Link to Publication Site) ● Publication site (DOI): 10.1016/j.femsle.2004.11.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15621433 ● Search Scopus @ Elsevier (PMID): 15621433 ● Search Scopus @ Elsevier (DOI): 10.1016/j.femsle.2004.11.005 (DOI: 10.1016/j.femsle.2004.11.005, PubMed: 15621433)
48.	Taniguchi Kazuko, Tsuneko Ono, Keiji Murakami, Darija Viducic, Kayama Sizuo, Katsuhiko Hirota, Ken Nemoto and Yoichiro Miyake : Novel Pseudomonas aeruginosa gene that suppresses tolerance to carbapenems, Antimicrobial Agents and Chemotherapy, Vol.47, No.9, 2997-3001, 2003. (Summary) A biapenem-tolerant mutant of Pseudomonas aeruginosa was isolated by Tn1737KH insertion. The survival of the mutant 3 h after the addition of biapenem was about 1000 times greater than that of the wild type. The mutant was also tolerant to other biapenems, such as imipenem, panipenem, and meropenem. (Keyword) Animals / Carbapenems / Colony Count, Microbial / DNA Primers / DNA Transposable Elements / Drug Resistance, Bacterial / Mice / knockout mice / Microbial Sensitivity Tests / Plasmids / Pseudomonas aeruginosa (Link to Publication Site) ● Publication site (DOI): 10.1128/AAC.47.9.2997-3001.2003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12937012 ● Search Scopus @ Elsevier (PMID): 12937012 ● Search Scopus @ Elsevier (DOI): 10.1128/AAC.47.9.2997-3001.2003 (DOI: 10.1128/AAC.47.9.2997-3001.2003, PubMed: 12937012)
49.	Atsushi Tabata, Hideaki Nagamune, Takuya Maeda, Keiji Murakami, Yoichiro Miyake and Hiroki Kourai : Correlation between resistance of Pseudomonas aeruginosa to quaternary ammonium compounds and expression of outer membrane protein OprR, Antimicrobial Agents and Chemotherapy, Vol.47, No.7, 2093-2099, 2003. (Summary) 論文題目:緑膿菌の細胞膜タンパク質OprRの発現と第四アンモニウム塩に対する耐性化の相関第四アンモニウム塩系消毒剤に耐性化した緑膿菌において顕著に発現量が増加する約25.6kDaの蛋白質を2次元電気泳動で分離し，そのN末端アミノ酸配列の解析によって，それが外膜蛋白質のOprRであることを明らかとした．またその耐性化株でOprRのノックアウト株を作成したところ，第四アンモニウム塩系消毒剤に対する感受性が野生株と同程度まで上昇することから，OprRがこの消毒薬耐性に重要な役割を果たしていることを示した． (Keyword) Adaptation, Physiological / Amino Acid Sequence / Bacterial Outer Membrane Proteins / Drug Resistance, Bacterial / Gene Deletion / Genes, Bacterial / Molecular Sequence Data / Mutagenesis / Pseudomonas aeruginosa / Quaternary Ammonium Compounds (Tokushima University Institutional Repository) ● Metadata: 117786 (Link to Publication Site) ● Publication site (DOI): 10.1128/AAC.47.7.2093-2099.2003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12821452 ● Search Scopus @ Elsevier (PMID): 12821452 ● Search Scopus @ Elsevier (DOI): 10.1128/AAC.47.7.2093-2099.2003 (Tokushima University Institutional Repository: 117786, DOI: 10.1128/AAC.47.7.2093-2099.2003, PubMed: 12821452)
50.	Ken Nemoto, Katsuhiko Hirota, Keiji Murakami, Kazuko Taniguti, Hiromi Murata, Darija Viducic and Yoichiro Miyake : Effect of varidase (streptodornase) on biofilm formed by Pseudomonas aeruginosa, Chemotherapy, Vol.49, No.3, 121-125, 2003. (Summary) The biofilm of Pseudomonas aeruginosa could be removed by Varidase (streptodornase) that was used as defibrinating drug. After cultivating the biofilm on a silicone chip in a modified alginate-producing medium in vitro, it was treated with Varidase or DNase I. In both treatments, the biofilm was removed depending on the concentration of the reagents. Varidase was apparently effective under the condition that the biofilm was exposed to more than 625 U/ml (a quarter of the concentration of the medical use) for 3 h, twice, at 37 degrees C. The result of this experiment indicates that (a) the DNases, DNase I and Varidase, were effective in destroying the biofilm of P. aeruginosa in vitro, and (b) in a clinical field, Varidase could be useful for P. aeruginosa focal infection, such as urinary tract infection, by removing the biofilm. (Keyword) Alginates / Biofilms / Cell Culture Techniques / Culture Media / Deoxyribonuclease I / Dose-Response Relationship, Drug / Humans / Pseudomonas Infections / Pseudomonas aeruginosa / Urinary Tract Infections (Link to Publication Site) ● Publication site (DOI): 10.1159/000070617 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12815204 ● Summary page in Scopus @ Elsevier: 2-s2.0-0038647338 (DOI: 10.1159/000070617, PubMed: 12815204, Elsevier: Scopus)
51.	Keiji Murakami : 緑膿菌におけるストレス反応と抗菌薬抵抗性, Shikoku Dental Research, Vol.14, No.1, 163-175, 2001. (Summary) 感染症の治療において，起炎菌に対するMICを基準にした適切な抗菌薬を選択したにも関わらず，十分な効果が得られないことも少なくない．この原因には，殺菌的抗菌薬を用いても，薬剤に対する抵抗性が上昇しているために，殺菌的効果が得られていない可能性が考えられる．緑膿菌PAOI株では，カルパペネム系抗菌薬であるbiapenemに対し，浮遊菌でのMBCに比べ付着菌では128倍高いMBC^ADを示した．また浮遊菌においても，定常期の細菌は，対数増殖期のそれよりも抵抗性を示し，heat shockにおいても抗菌薬抵抗性が上昇することが明らかになった． (Keyword) 緑膿菌 / ストレス反応 / 抗菌薬抵抗性 / 付着
52.	Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono, Kinya Murakami, Keiji Murakami, Daisuke Nagao and Yoichiro Miyake : Effect of varidase (streptokinase) on biofilm formed by Staphylococcus aureus, Chemotherapy, Vol.46, No.2, 111-115, 2000. (Summary) Staphylococcus aureus forms a fibrin-rich biofilm in the presence of plasma which is highly resistant to attack by the human immune system and to chemotherapy. Varidase, composed mainly of streptokinase, is used for hydrolyzing clots. In this study, we attempted to destroy the biofilm of S. aureus with Varidase and to apply this drug in the treatment of staphylococcal infections. Four clinical isolates were used in the experiments. These organisms formed a several-millimeter-thick biofilm on type IV collagen coated coverslips in trypticase soy broth containing 50% human plasma. The biofilm was composed of bacterial cell which adhered to fibrillar fibers and of sediment derived from plasma. 10,000 U/ml of Varidase, the dose which is used clinically, removed the sediment and reduced the number of live bacteria in biofilms to less than 20% of control. 200 U/ml of Varidase was also effective against biofilms of the organisms. An equal combination of Varidase and ofloxacin had an additive effect on the bacteria. The results of this study demonstrate that Varidase is highly effective in destroying biofilms of S. aureus in vitro and suggest that this drug would be useful for treating staphylococcal infections. (Keyword) Staphylococcus Aureus / Biofilm / Varidase / Ofloxacin / Resistance (Link to Publication Site) ● Publication site (DOI): 10.1159/000007264 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10671761 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033953104 (DOI: 10.1159/000007264, PubMed: 10671761, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に対する新規化合物の作用機序, Bacterial Adherence & Biofilm, Vol.31, 2018.
2.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 新規化合物によるレボフロキサシン及びトブラマイシン殺菌作用の増強効果, Bacterial Adherence & Biofilm, Vol.30, 2017.
3.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, Takashi Amoh and Yoichiro Miyake : Streptococcus intermedius biofilm componentsの糖鎖結合能と炎症反応誘導能に関する解析, Bacterial Adherence & Biofilm, Vol.29, 2016.
4.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 新規化合物によるビアペネム殺菌作用の増強効果について, Bacterial Adherence & Biofilm, Vol.29, 2016.
5.	Keiji Murakami, Takashi Amoh, Katsuhiko Hirota and Yoichiro Miyake : クラリスロマイシンによる緑膿菌c-di-GMPの誘導, 第50回緑膿菌感染症研究会講演記録 /緑膿菌感染症研究会事務局編, 2016.
6.	Katsuhiko Hirota, Hiromichi Yumoto, Yumi Hoshimo, Keiji Murakami, 宮本幸治, Takashi Matsuo and Yoichiro Miyake : 水溶性MPCポリマーの口腔細菌付着抑制効果, Bacterial Adherence & Biofilm, Vol.24, 47-49, 2011. (Summary) 口腔細菌によるbiofilm，すなわちdental plaqueの形成にはいくつかのkey stepがあり，dental plaque形成の抑制のためにはそれらのkey stepに効果的に働く方法を選択する必要が有る．我々は，超親水性表面を得ることができる2-methacryloloxethyl phosphorylcholine(MPC)co-polymerを用いてプラスチック表面をコートした界面は微生物の付着抑制に関与することを報告してきた．本実験では5%水溶性MPCポリマーで処理したHydroxyapatite(HY)プレートと培養歯肉上皮細胞(RT-7)へのStreptococcus mutansの付着状況を顕微鏡下にて観察した．その結果，5%水溶性MPCポリマー処理でHYプレート及び培養歯肉上皮細胞上へのS.mutansの付着は抑制されることが示された．以上よりHYプレートや培養歯肉上皮細胞に吸着した水溶性MPCポリマーは，プラスチックへのコーティングと同様にS.mutansの付着抑制効果を発揮することが示唆された．
7.	Keiji Murakami and Yoichiro Miyake : 緑膿菌臨床分離株におけるRSCVsの分離とその性状について, Bacterial Adherence & Biofilm, Vol.24, 81-83, 2011. (Summary) 緑膿菌感染症において，寒天培地上で小さな皺上のコロニー性状を示す，rugose small colony variants(RSCVs)の存在が報告されている．このRSCVsは，細胞内のセカンドメッセンジャーであるc-di-GMPの細胞内濃度が上昇しているためであると考えられている．今回我々は，徳島大学病院で分離された緑膿菌30株についてRSCVsの有無を検討したところ，2株が小さな皺状のコロニー性状を示し，バイオフィルム形性能が高く，運動性も低下していたことから，RSCVsであると考えられる．そのうちの1株は，c-di-GMP合成に関与する遺伝子オペロンの1つであるwspF遺伝子の変異の結果である事が明らかとなった．もう1株では，wspF遺伝子には大きな変異は見られなかった．これらの結果から，臨床分離株30株中2株のRSCVsが確認されたものの，その原因となる遺伝子は異なっていることが明らかとなった．
8.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono, Hideaki Nakae and Yoichiro Miyake : 付着緑膿菌の抗菌薬抵抗性とQuorum sensing機構について, Bacterial Adherence & Biofilm, Vol.20, 110-115, 2006. (Keyword) PPseudomonas aeruginosa / Quorum sensing system / Antibiotic tolerance / Biapenem
9.	Katsuhiko Hirota, Keiji Murakami, 鹿山鎮男, Ken Nemoto and Yoichiro Miyake : 微生物付着に与える2-methacryloyloxyethyl phosphorylcholine co-polymer処理の影響, Bacterial Adherence & Biofilm, Vol.17, 12-15, 2003. (Keyword) 2-methacryloyloxyethyl phosphorylcholine co-polymer / Superhydrophilicity / Microbial Adherence
10.	Katsuhiko Hirota, Keiji Murakami, Ken Nemoto and Yoichiro Miyake : Streptococcus intermediusの付着，凝集時におけるhistone-like proteinの局在, Bacterial Adherence & Biofilm, Vol.16, 27-32, 2002. (Keyword) tone-like protein / Localization / Streptococcus Intermedeus / Adherence

Academic Letter:

1.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Biological Roles of Extracellular DNA in Bacterial Infection, Asean Plus and Tokushima Joint International Conference, Program and Proceeding Book, 47-48, 2012.
2.	Katsuhiko Hirota, Takeyoshi Yoneyama, Mayumi Sakamoto, Hiroshi Miyamoto, Masanori Kurihara, Shizuo Kayama, Keiji Murakami, Hiromichi Yumoto, Takashi Matsuo and Yoichiro Miyake : High prevalence of Pseudomonas aeruginosa from oropharyngeal biofilm in patients with cerebrovascular infarction and dysphagia., Chest, Vol.138, No.1, 237-238, 2010. (Keyword) Aged / Biofilms / Cerebral Infarction / Deglutition Disorders / female / Humans / male / Oropharynx / Pneumonia, Aspiration / Prevalence / Pseudomonas Infections / Pseudomonas aeruginosa (Link to Publication Site) ● Publication site (DOI): 10.1378/chest.10-0240 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20605833 ● Search Scopus @ Elsevier (PMID): 20605833 ● Search Scopus @ Elsevier (DOI): 10.1378/chest.10-0240 (DOI: 10.1378/chest.10-0240, PubMed: 20605833)

Review, Commentary:

1.	Hiromichi Yumoto, Katsuhiko Hirota, Yoichiro Miyake, Keiji Murakami, Natsumi Fujiwara, 秋月皆人 and Hideki Fujii : ``撥菌''∼口腔バイオフィルム感染症予防への応用∼, The Journal of Educational Conference on All Japan Colleges of Dental Hygiene, Vol.10, No.25, 13-17, Mar. 2021. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980706066501120 (CiNii: 1521980706066501120)
2.	Keiji Murakami and Hideki Fujii : Risk of cross-infection of drug-resistant bacteria in dental practice, Journal of Oral Health and Biosciences, Vol.30, No.2, 67-68, Feb. 2018. (Tokushima University Institutional Repository) ● Metadata: 111072 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.30.2_67 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.30.2_67 (Tokushima University Institutional Repository: 111072, DOI: 10.20738/johb.30.2_67)
3.	Keiji Murakami and Yoichiro Miyake : バイオフィルム形成菌の抗菌薬抵抗性「特集 ''One Health''時代の耐性菌対策・研究, Antibiotics and Chemotherapy, Vol.33, No.5, 1024-1028, May 2017.
4.	Yoichiro Miyake and Keiji Murakami : 付着緑膿菌の抗菌薬抵抗性, Antibiotics and Chemotherapy, Vol.31, No.9, 120-125, 2015.
5.	Momoyo Azuma and Keiji Murakami : 感染症とは, 歯界展望(別冊), 167-172, May 2014.
6.	Keiji Murakami and Yoichiro Miyake : Regulation for bacterial function by macrolide, Respiratory Medicine, Vol.24, No.4, 397-399, Oct. 2013. (Keyword) macrolide / Pseudomonas aeruginosa / quorum sensing / virulence / biofilm (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291856152869248 (CiNii: 1520291856152869248)
7.	Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : Regulatory networks for antibiotic tolerance and biofilm formation in Pseudomonas aeruginosa, Nihon Saikingaku Zasshi, Vol.67, No.2, 227-243, May 2012. (Summary) <i>Pseudomonas aeruginosa</i>はcompromised hostにしばしば難治性慢性感染症を惹起する．その主な要因として，バイオフィルム形成能が高く抗菌薬に対する抵抗性が高いことが挙げられる．近年バイオフィルム形成のメカニズムについてはquorum sensing(QS)システム(密度感知機構)やcyclic di-guanosine monophosphate(c-di-GMP)等のグローバルレギュレーターの関与が明らかになり，また共焦点レーザー蛍光顕微鏡を用いたバイオフィルム内の遺伝子発現と形態的解析が進み，生理的性状の異なる多様な細胞集団で構成された多細胞生物的な構造を形成することが明らかになってきた．しかし抗菌薬抵抗性のメカニズムについては，まだその詳細は明らかではない．これまでに浮遊状態の細菌は，環境中の栄養源，pH，アルコール，浸透圧や菌体内代謝産物など各種のストレスを感知し，副次的ς因子やQSを介して，固相表面に付着しマイクロコロニーさらに菌体外マトリクスを形成することによりバイオフィルムへと移行し，各種の環境ストレスに対する抵抗性が上昇する．本稿では，<i>P. aeruginosa</i>のRpoS, RpoN等のストレス関連ς因子やQSおよびc-di-GMPなどのセカンドメッセンジャーと抗菌薬抵抗性との関連性について，<i>P. aeruginosa</i>のライフサイクルとの関わりを含めて，最近の知見を中心に概説する．<br> (Keyword) Animals / Anti-Bacterial Agents / Bacterial Adhesion / Bacterial Proteins / Biofilms / Cyclic GMP / Drug Resistance, Bacterial / Extracellular Matrix / Life Cycle Stages / Pseudomonas aeruginosa / Quorum Sensing / RNA Polymerase Sigma 54 / Second Messenger Systems / Sigma Factor (Link to Publication Site) ● Publication site (DOI): 10.3412/jsb.67.227 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22688178 ● CiNii @ National Institute of Informatics (CRID): 1390001206454468864 ● Search Scopus @ Elsevier (PMID): 22688178 ● Search Scopus @ Elsevier (DOI): 10.3412/jsb.67.227 (DOI: 10.3412/jsb.67.227, PubMed: 22688178, CiNii: 1390001206454468864)
8.	Keiji Murakami : New bacterial second messenger, c-di-GMP, Respiratory Medicine, Vol.19, No.1, 66-70, Jan. 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520854806105792256 (CiNii: 1520854806105792256)
9.	Yoichiro Miyake and Keiji Murakami : バイオフィルム形成とクオラムセンシング臨床医学編口腔内感染症とバイオフィルム, Antibiotics and Chemotherapy, Vol.26, No.9, 66-70, 2010.
10.	Keiji Murakami and Yoichiro Miyake : 口腔細菌とQuorum sensing, Shikoku Dental Research, Vol.15, No.2, 251-256, Jan. 2003.

Proceeding of International Conference:

1.	Keiji Murakami : Role of psl gene and antioxidant ability for antibioitic tolerance in Pseudomonas aeruginosa, ERTO-MiCS International Symposium on Sociomicrobiology, Jul. 2019.
2.	Natsumi Fujiwara, Hiromichi Yumoto, Keiji Murakami, Yasusei Kudo, Hiromi Nakae, Katsuhiko Hirota, Kazumi Ozaki and Yoichiro Miyake : 2-methacryloyloxyethyl-phosphorylcholine (MPC)-polymer suppresses the adherence of oral bacteria, 2018 IADR/PER General Session (ExCel London Convention Center, London, England) 25-28th July, 2018, Jul. 2018.
3.	Susilowati Heni, Keiji Murakami, Takashi Amoh, Katsuhiko Hirota, Yoichiro Miyake, Hiromichi Yumoto and Takashi Matsuo : Royal Jelly inhibits Pseudomonas aeruginosa adherence and reduces excessive inflammatory resoponses in human epithelial cells, 2016 IADR, Seoul, Jun. 2016.
4.	Hiromichi Yumoto, Takashi Matsuo, Katsuhiko Hirota, Kouji Hirao, Miyazaki Tsuyoshi, Keiji Murakami, Natsumi Fujiwara and Yoichiro Miyake : Anti-inflammatory and protective effects of 2-methacryloyloxyethyl-phosphorylcholine-polymer on oral epithelial cells, 92th General Session & Exhibition of the International Association for Dental Research (Cape Town, South Africa), Jun. 2014.
5.	Nur Ashikin, Hiromichi Yumoto, Keiji Murakami, Katsuhiko Hirota, 天羽崇 and Yoichiro Miyake : Extracellular DNA affects Streptococcus mutans biofilm through quorum sensing system and histone-like DNA binding protein expression, The 12th Japan-Korea International Symposium on Microbiology, Tokyo, Mar. 2014.
6.	Hiromichi Yumoto, Katsuhiko Hirota, Kouji Hirao, Keiji Murakami, Yoichiro Miyake and Takashi Matsuo : Pathogenic roles of Streptococcal histone-like protein in microbial infection, The 15th Joint Scientific Meeting of JSCD-KACD (Gyeongju, Korea), Nov. 2013.
7.	Momoyo Azuma, Keiji Murakami, Katuhiko Hirota, Tsuneko Ono, Yoichiro Miyake and Yasuhiko Nishioka : The relationship between antibiotic tolerance and severity of clinical isolated Pseudomonas aeruginosa in respiratory disease patients, The28th International Congress of Chemotherapy and Infection and the 14th Asia-pacific Society of Clinical Microbiology and Infection, 横浜, Jun. 2013.
8.	Keiji Murakami, Momoyo Azuma, Katsuhiko Hirota, Tsuneko Ono, Nishida Yasuhiko and Yoichiro Miyake : The correlation between antibiotic tolerance and virulence of Pseudomonas aeruginosa clinical isolates, 28th International Congress of Chemoteherap and Infection, Yokohama, Jun. 2013.
9.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Biological Roles of Extracellular DNA in Bacterial Infection, Asean Plus and Tokushima Joint International Conference, Yogyakarta, Dec. 2012.
10.	Keiji Murakami, Darija Viducic, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : Pseudomonas aeruginosa psl genes play an important role in biapenem tolerance, International Union of Microbiological Societies 2011 Congress, Sapporo, Sep. 2011.
11.	Darija Viducic, Keiji Murakami, Tsuneko Ono and Yoichiro Miyake : The Pseudomonas aeruginosa quinolone signal plays a dual role in the response to antimicrobial agents, International Union of Microbiological Societies 2011 Congress, Sapporo, Sep. 2011.
12.	Katsuhiko Hirota, Hiromichi Yumoto, Nur Asikin, Kouji Hirao, Kanako Takahashi, Liu Dali, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Gene Expression Profiling of Human Monocytic THP-1 Cells Stimulated With Extracellular Streptococcus intermedius Histone-Like DNA Binding Protein, International Union of Microbiological Societies 2011 Congress, Sep. 2011.
13.	Keiji Murakami, Darija Viducic, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : The involvement of psl genes and the second messenger c-di-GMP in antibiotic tolerance of adherent Pseudomonas aeruginosa, EUROBIOFILMS 2011 -Second European Congress on Microbial Biofilms-Basic and Dlinical Aspedts-, Copenhagen, Jul. 2011.
14.	Katsuhiko Hirota, M Hori, S Hayakawa, Keiji Murakami and Yoichiro Miyake : Development of New Materials That Refuse Microbial Adherence, EUROBIOFILMS 2011 -Second European Congress on Microbial Biofilms-Basic and Dlinical Aspedts-, Copenhagen, Jul. 2011.
15.	Keiji Murakami and MR Parsek : The Regulation of Pel Transcription in Tuve Biofilm, ASM Conferences: Biofilms 2009, Cancun, Mexico, Nov. 2009.
16.	Susilowati Heni, Hirohiko Okamura, Katsuhiko Hirota, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji and Yoichiro Miyake : The molecular mechanism for Streptococcus intermedius intermedilysin-induced cell death inhuman cholangiocellular carcinoma cells, International Joint Symposium Frontier in Biomedical Sciences: From Genes to Applications, Yogyakarta, Nov. 2008.
17.	Hiromichi Yumoto, Liu Dali, Keiji Murakami, Katsuhiko Hirota, Hideaki Nagamune, Shizuo Kayama, Takashi Matsuo and Yoichiro Miyake : Gene-regulatory and Physiological Functions of Histone-like Protein from Streptococci, 86th General Session and Exhibition of the International Association for Dental Research, Toronto (Canada), Jul. 2008.
18.	Susilowati Heni, Hirohiko Okamura, Katsuhiko Hirota, Kaya Yoshida, Keiji Murakami, Hideaki Nagamune, Tatsuji Haneji and Yoichiro Miyake : NFAT1 activation in intermedilysin-induced human cholangiocellular carcinoma cell HuCCT1, The 2nd International Symposium on "The Future Direction of Oral Sciences in the 21st Century", Tokushima, Dec. 2007.
19.	Liu Dali, Hiromichi Yumoto, Keiji Murakami, Katsuhiko Hirota, Shizuo Kayama, Takashi Matsuo and Yoichiro Miyake : The essentiality and involvements of streptocuccus intermedius histone-like protein in bacterial viability and normal growth, The 2nd International Symposium on "The Future Direction of Oral Sciences in the 21st Century", Tokushima, Dec. 2007.
20.	Heni Susilowati, Katsuhiko Hirota, Hirohiko Okamura, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji and Yoichiro Miyake : Intermedilysin induces cell death in HepG2 cells, 21st International Association for Dental Research - South East Asia Division, Bali, Indonesia, Sep. 2007.
21.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : Role of quorum sensings system of adherent pseudomonas aeruginosa in antibiotic tolerance, ASM conferences Pseudomonas 2007, Seattle, Aug. 2007.
22.	Tomoko Kimura, Kazumi Ozaki, Keiji Murakami, Kikumi Fujisaka and Takashi Matsuo : The Analysis of role of Phosphoenolpyruvate-Dependent Sucrose Phosphotransferase System in pathogenicity of Streptococcus mutans., 第1回国際シンポジウム・FDワークショップ, Awaji, Mar. 2007.
23.	Liu Dali, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota and Yoichiro Miyake : Investigation of the toxicity of Streptococcus intermedius histone-like protein in Escherichia coli, The 1st international symposium and workshop ''The Future Direction of Oral Sciences in the 21st century'', Awajishima, Mar. 2007.
24.	Heni Susilowati, Katsuhiko Hirota, Hirohiko Okamura, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji and Yoichiro Miyake : The mechanisms of Intermedilysin to induce cell death on HepG2 and HuCCT1 cell lines, The 1st international symposium and workshop ''The Future Direction of Oral Sciences in the 21st century'', Awajishima, Mar. 2007.
25.	LIU Dali, Katsuhiko Hirota, Keiji Murakami and Yoichiro Miyake : pathogenicity of streptococcus intermedius,an Oral Commensal Bacterium, 2005-SINO-JAPANESE CONFERENCE ON STOMATOLOGY, Shanghai, Nov. 2005.
26.	Keiji Murakami, Kayama Sizuo, Viducic Darija, Tsuneko Ono and Yoichiro Miyake : The involvement of pslL gene in biapenem tolerance of Pseudomonas aeruginosa, Pseudomonas 2005 10th International Congress Abstract Book, 139, Marseille, Aug. 2005.
27.	Darija Viducic, Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : A role of ppGpp in tolerance to quinolone in Pseudomonas aeruginosa, Pseudomonas 10th International congress Abstract Book, 101, Marseille, Aug. 2005.
28.	Hiromichi Yumoto, Katsuhiko Hirota, Hideaki Nagamune, Kazuto Ohkura, Keiji Murakami, Masayoshi Yamada, Hideaki Nakae, Yoichiro Miyake and Takashi Matsuo : Molecular analysis of histone-like protein from Streptococcus intermedius, 80th General Session and Exhibition of the International Association for Dental Research, San Diego(USA), Mar. 2002.
29.	Naoki Ohmura, Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Hideo Kanitani, Toshiya Kashiwabara, Yoichiro Miyake and Tetsuo Ichikawa : Influence of denture plaque on the pharyngeal microflora, 80th General Session and Exhibition of the International Association for Dental Research, San Diego(USA), Mar. 2002.

Proceeding of Domestic Conference:

1.	Muhammad Reza Pahlevi, Keiji Murakami, Murata Rina and Hideki Fujii : Identification of antibiotic tolerance related genes to AIA-1 in Pseudomonas aeruginosa, 93,
2.	関田泰子, Keiji Murakami, Takashi Amoh, Natsumi Fujiwara and Hiromichi Yumoto : 災害時におけるドクダミ茶の口腔ケアへの有効利用, 第20回日本医療マネジメント学会高知県支部学術集会, Aug. 2024.
3.	関田泰子, Keiji Murakami, Takashi Amoh, Natsumi Fujiwara and Hiromichi Yumoto : 南海トラフ地震直後の感染症予防のためのドクダミの有効利用の検討, 第62回日本薬学会・日本薬剤師会・日本病院薬剤師会中四国支部学術大会, Oct. 2023.
4.	仲村大輔, 植村勇太, Yuka Hiroshima, Keiji Murakami, Akikazu Murakami and Hiromichi Yumoto : Porphyromonas gingivalis 由来OMVsは破骨細胞の分化と歯槽骨吸収に関与する, 第75回日本細菌学会中国・四国支部総会(岡山・WEB), Oct. 2022.
5.	SATOH Tomomi, Yuka Hiroshima, Akikazu Murakami, Hideki Fujii, Akiko Sakurai, Keiko Kataoka and Keiji Murakami : カタラーゼをコードするkatA/katB遺伝子が及ぼす緑膿菌の抗菌薬抵抗性における影響, 第45回徳島県医学検査学会, Dec. 2021.
6.	秋月皆人, 植村勇太, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : 歯周病原細菌とその線毛TypeのPCRによる迅速検出システムの有効性の検討, 第74回日本細菌学会中国・四国支部総会, Oct. 2021.
7.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis OMVによる歯肉上皮細胞のサイトカイン産生機構, 第74回日本細菌学会中国・四国支部総会, Oct. 2021.
8.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, Yuji Inagaki, Hiromichi Yumoto and Hideki Fujii : ヒト歯肉上皮細胞におけるPorphyromonas gingivalis由来メンブレンベシクルの炎症性サイトカイン産生誘導機構の解明, 第19回四国免疫フォーラム, Jun. 2021.
9.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 第73回日本細菌学会中国・四国支部総会, 32, Oct. 2020.
10.	Pahlevi Reza Muhammad, Keiji Murakami, Yuta Kita, Rina Murata, Yuka Hiroshima and Hideki Fujii : Screening for the genes influenced by AIA-1 in Pseudomonas aeruginosa, 第73回日本細菌学会中国・四国支部総会, 31, Oct. 2020.
11.	AKIZUKI Minato, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングにおけるTi表面への歯周病原菌付着抑制効果の検討, 第73回日本細菌学会中国・四国支部総会, 30, Oct. 2020.
12.	Yuta Kita, Pahlevi Reza Muhammad, Rina Murata, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : バイオフィルム形成緑膿菌におけるPA2384遺伝子の役割について, 第73回日本細菌学会中国・四国支部総会, 29, Oct. 2020.
13.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 第73回日本細菌学中国・四国支部総会, 22, Oct. 2020.
14.	Muhammad Reza Pahlevi, Keiji Murakami and Hideki Fujii : Screening for antibiotic tolerance factor of Pseudomonas aeruginosa, 第62回歯科基礎医学会学術大会, Sep. 2020.
15.	Keiji Murakami, 村田梨菜, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加による酸化ストレスについて, 第54回緑膿菌感染症研究会, Feb. 2020.
16.	Keiji Murakami and Hideki Fujii : 緑膿菌におけるc-di-GMPによるバイオフィルム形成の制御, 第93回日本細菌学会総会, Feb. 2020.
17.	村田梨菜, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加による酸化ストレス反応について, 第93回日本細菌学会総会, Feb. 2020.
18.	岡本舞, Yuta Kita, Rina Murata, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌におけるバイオフィルム形成菌の抗菌薬抵抗性について, 徳島県歯科医学大会, Feb. 2020.
19.	Rina Murata, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加と酸化ストレスについて, 徳島県歯科医学大会, Feb. 2020.
20.	喜田悠太, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : 緑膿菌におけるバイオフィルム形成菌の抗菌薬抵抗性に関わる遺伝子について, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
21.	藤本望, 村田梨菜, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 亜硝酸イオンの口腔内における生理的意義について, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
22.	村田梨菜, 藤本望, Keiji Murakami, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加と酸化ストレスについて, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
23.	Keiji Murakami, 喜田悠太, 村田梨菜, Yuka Hiroshima, Keiko Kataoka and Hideki Fujii : 緑膿菌バイオフィルム形成菌の抗菌薬抵抗性に関わる遺伝子について, 第33回日本バイオフィルム学会学術集会, Jul. 2019.
24.	Keiji Murakami, 天羽崇, Keiko Kataoka and Hideki Fujii : The correlation between antibiotic tolerance and antioxidant ability in Pseudomonas aeruginosa, The 92nd Annual Meeting of Japanese Society for Bacteriology, Apr. 2019.
25.	藤本望, 村田梨菜, Keiji Murakami, Hideki Fujii, Licht Miyamoto, 井上貴久, Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa and Shuichi Hamano : 唾液中の硝酸イオンが口腔細菌に与える影響について·, 第42回徳島県医学検査学会, Dec. 2018.
26.	Rina Murata, Keiji Murakami, Hideki Fujii, 佐藤雅美, 笹田倫子, 井上みなみ, 平尾早紀, 別所将弘, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 呼吸器感染症患者由来緑膿菌の抗菌薬抵抗性と抗酸化能の関連について, 第42回徳島県医学検査学会, Dec. 2018.
27.	Natsumi Fujiwara, Keiji Murakami, Kaya Yoshida, Yasusei Kudo, Katsuhiko Hirota, Kazumi Ozaki, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングによる義歯用レジンのカンジダ付着(撥菌)効果, 第60回日本歯科基礎医学会学術大会 2018年9月5-7日(九州大学病院キャンパス百年講堂, 福岡市), Sep. 2018.
28.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳, Yoichiro Miyake and Hideki Fujii : 浮遊菌とバイオフィルム形成菌の抗菌薬抵抗性に対するrpoS遺伝子の役割, 第32回日本バイオフィルム学会学術集会, Jul. 2018.
29.	Keiji Murakami, Takashi Amoh, Keiko Kataoka, 狩山玲子, Katsuhiko Hirota, Yoichiro Miyake and Hideki Fujii : 緑膿菌オートインデューサーアナログのマクロライドに対する効果, 第91回日本細菌学会総会, Mar. 2018.
30.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, Yoichiro Miyake and Hideki Fujii : 緑膿菌rpoS遺伝子が抗菌薬抵抗性に及ぼす役割, 第91回日本細菌学会総会, Mar. 2018.
31.	谷脇竜弥, 杉田知世, Keiji Murakami, Takashi Amoh, Atsushi Tabata, Yoshiko Yamamura, Tetsuya Tamatani, Hideaki Nagamune, Youji Miyamoto and Hideki Fujii : 幼児口腔内創部より検出された多剤耐性レンサ球菌について, 四国歯学会第52回例会, Mar. 2018.
32.	Fujiwara Noriko, Satoh Masami, Keiji Murakami and Momoyo Azuma : 総合周産期母子医療センターにおける感染対策について, 第33回環境感染学会総会, Feb. 2018.
33.	Keiji Murakami, Kariyama Reiko, Kumon Hiromi and Yoichiro Miyake : 緑膿菌Autoinducer Analogがマクロライドの抗菌作用に及ぼす影響について, 第52回緑膿菌感染症研究会, Feb. 2018.
34.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, Yoichiro Miyake and Hideki Fujii : rpoS遺伝子が緑膿菌の抗菌薬抵抗性に及ぼす影響, 第70回日本細菌学会中国・四国支部総会, Oct. 2017.
35.	Natsumi Fujiwara, Hiromichi Yumoto, Katsuhiko Hirota, Keiji Murakami and Kazumi Ozaki : Suppression of oral bacteria by 2-methacryloyloxyethyl-phosphorylcholine-polymer, 第59回歯科基礎医学会学術大会プログラム・抄録集平成29年9月16-18日(松本歯科大学，長野県塩尻市), 341, Sep. 2017.
36.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に対する新規化合物の作用機序, 第31回日本バイオフィルム学会学術集会, Jul. 2017.
37.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌における新規化合物の抗菌薬抵抗性に対する作用機序の解析, 第90回日本細菌学会総会, Mar. 2017.
38.	Keiji Murakami, Takashi Amoh, Katsuhiko Hirota, Keiko Kataoka and Yoichiro Miyake : 緑膿菌呼吸器感染症における抗菌薬抵抗性の臨床的重要性について「シンポジウム不均一性細菌学:表現型の不均一性に基づいた細菌の生存戦略」, 第90回日本細菌学会総会, Mar. 2017.
39.	Keiji Murakami, 狩山玲子, 公文裕巳 and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に及ぼすAutoinducer Analogの作用機序について, 第51回緑膿菌感染症研究会, Feb. 2017.
40.	Shoto Ogawa, Shinichi Fujie, Keiji Murakami, Takashi Amoh, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 緑膿菌オートインデューサー類似化合物が抗菌薬抵抗性に及ぼす影響, 第40回徳島県医学検査学会, Dec. 2016.
41.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 新規化合物の作用機序およびバイオフィルムに対する効果, 第69回日本細菌学会中国・四国支部総会, 38, Oct. 2016.
42.	Natsumi Fujiwara, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota and Yoichiro Miyake : 歯周病原菌に対する新規化合物の効果, 第69回日本細菌学会中国・四国支部総会平成28年10月15-16日香川県高松市かがわ国際会議場, 38, Oct. 2016.
43.	Natsumi Fujiwara, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota, Kazumi Ozaki and Yoichiro Miyake : Effects of novel compounds on periodontopathic bacteria, 第58回歯科基礎医学会学術大会北海道札幌市 2016年8月24-26日, Aug. 2016.
44.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 新規化合物によるレボフロキサシン及びトブラマイシン殺菌作用の増強効果, 第30回バイオフィルム学会学術集会, Jul. 2016.
45.	Keiji Murakami : 緑膿菌呼吸器感染症における抗菌薬抵抗性の重要性について, 第1回バイオフィルム研究者若手ワークショップ, Jul. 2016.
46.	Kazuto Shiraishi, Keiji Murakami, Noriko Saito-Tarashima, Kazuhiro Furukawa, Yoichiro Miyake and Noriaki Minakawa : ホスホジエステラーゼ抵抗性を有する4'-チオ化学修飾型環状ジヌクレオチドの合成と評価, 日本薬学会第136年会, Mar. 2016.
47.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, Takashi Amoh and Yoichiro Miyake : 口腔常在菌Streptococcus intermediusが呼吸器疾患重症化に関与するメカニズム, 第89回日本細菌学会総会, Mar. 2016.
48.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 新規化合物が耐性菌やバイオフィルムに及ぼす影響, 第89回日本細菌学会総会, Mar. 2016.
49.	Keiji Murakami, Takashi Amoh, Katsuhiko Hirota and Yoichiro Miyake : 付着菌およびバイオフィルム形成菌の抗菌薬抵抗性とそのメカニズム, 第89回日本細菌学会総会, Mar. 2016.
50.	Keiji Murakami, Takashi Amoh, Katsuhiko Hirota and Yoichiro Miyake : クラリスロマイシンによる緑膿菌c-di-GMPの誘導, 第50回緑膿菌感染症研究会, Feb. 2016.
51.	Ayumi Yoshida, Mai Ueta, Keiji Murakami, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 緑膿菌におけるストレス応答と抗菌薬抵抗性について, 第39回徳島県医学検査学会, Dec. 2015.
52.	Mai Ueta, Ayumi Yoshida, Keiji Murakami, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : リボザイムを応用したcyclic-di-GMPの定量法の開発, 第39回徳島県医学検査学会, Dec. 2015.
53.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 緑膿菌AI類似化合物は緑膿菌に対するビアペネムの殺菌効果を増強する, 第63回日本化学療法学会西日本支部総会, Oct. 2015.
54.	Keiji Murakami, 狩山玲子, Takashi Amoh, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 緑膿菌psl遺伝子が抗菌薬抵抗に及ぼす影響, 第63回日本化学療法学会西日本支部総会, Oct. 2015.
55.	Takashi Amoh, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 新規化合物による抗菌薬殺菌作用の増強効果について, 第68回日本細菌学会中国・四国支部総会, Oct. 2015.
56.	Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌AHL類似化合物によるビアペネム殺菌効果の増強について, 第57回歯科基礎医学会学術大会, Sep. 2015.
57.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, Takashi Amoh and Yoichiro Miyake : Streptococcus intermedius biofilm componentsの糖鎖結合能と炎症反応誘導に関する解析, 第29回日本バイオフィルム学術集会, Jul. 2015.
58.	天羽崇, Keiji Murakami, 狩山玲子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 新規化合物によるビアペネム殺菌作用の増強効果について, 第29回日本バイオフィルム学会学術集会, Jul. 2015.
59.	白石和人, Keiji Murakami, Noriko Saito-Tarashima, Kazuhiro Furukawa, Yoichiro Miyake and Noriaki Minakawa : 糖部修飾型環状ジヌクレオチドの合成と評価, 創薬懇話会2015 in 徳島, Jul. 2015.
60.	白石和人, Keiji Murakami, Noriko Saito-Tarashima, Kazuhiro Furukawa, Yoichiro Miyake and Noriaki Minakawa : Cyclic-di-4'-S-adenosine monophosphate (c-di-SAMP)の合成と評価, 第17回プロセス化学東四国フォーラムセミナー, Jun. 2015.
61.	Keiji Murakami, 狩山玲子, 堀賢司, 光畑律子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 新規化合物が薬剤耐性緑膿菌に対する殺菌効果に及ぼす影響, 第63回日本化学療法学会総会, Jun. 2015.
62.	天羽崇, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に対する新規化合物の効果, 第88回日本細菌学会総会, Mar. 2015.
63.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, 天羽崇 and Yoichiro Miyake : Streptococcus intermedius Histone-Like Proteinと細胞外ベシクルの特性, 第88回日本細菌学会総会, Mar. 2015.
64.	Keiji Murakami, Hideaki Maseda, 天羽崇, Katsuhiko Hirota, Keiko Kataoka and Yoichiro Miyake : 臨床および環境分離緑膿菌の抗菌薬抵抗性と病原因子に関する検討, 第88回日本細菌学会総会, Mar. 2015.
65.	Yukari Yoshikawa, Shoko Kannuki, Keiji Murakami, Yoichiro Miyake, 畑美智子, 佐藤雅美, 笹田倫子, 香川葉子, 菅崎幹樹, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 本院で分離されたST-8型MRSAについて, 第38回徳島県医学検査学会, Dec. 2014.
66.	Shoko Kannuki, Yukari Yoshikawa, Keiji Murakami, Yoichiro Miyake, Hideaki Maseda, 畑美智子, 佐藤雅美, 笹田倫子, 香川葉子, 菅崎幹樹, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 臨床および環境分離緑膿菌における病原性について, 第38回徳島県医学検査学会, Dec. 2014.
67.	狩山玲子, 堀賢司, Keiji Murakami, 光畑律子, 和田耕一郎, 渡辺豊彦, Yoichiro Miyake and 公文裕巳 : OprD欠損緑膿菌によるマウス大腿部感染モデルに対するクオラムセンシング阻害剤とビアペネムの併用効果, 第62回日本化学療法学会西日本支部総会第57回日本感染症学会中日本地方会学術集会第84回日本感染症学会西日本地方会学術集会合同開催, Oct. 2014.
68.	Keiji Murakami, 狩山玲子, 堀賢司, 光畑律子, Katsuhiko Hirota, 公文裕巳 and Yoichiro Miyake : 緑膿菌におけるクオラムセンシング阻害剤が抗菌薬抵抗性に及ぼす影響, 第62回日本化学療法学会西日本支部総会第57回日本感染症学会中日本地方会学術集会第84回日本感染症学会西日本地方会学術集会合同開催, Oct. 2014.
69.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, 天羽崇, Takashi Matsuo and Yoichiro Miyake : Streptococcus intermedius Histone-Like DNA Binding Proteinの結合解析とExtracellular Vesicleとの関連, 第67回日本細菌学会中国・四国支部総会, Oct. 2014.
70.	天羽崇, Keiji Murakami, 狩山玲子, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に対する新規化合物の効果, 第67回日本細菌学会中国・四国支部総会, Oct. 2014.
71.	Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌臨床分離株における抗菌薬抵抗性と病原性との関連, 第56回歯科基礎医学会学術大会, Sep. 2014.
72.	Keiji Murakami : 付着菌における抗菌薬抵抗性とそのメカニズムについて, 第28回Bacterial Adherence & Biofilm学術集会, Jul. 2014.
73.	Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性と病原因子に関する検討, 第88回日本感染症学会学術講演会第62回日本化学療法学会総会合同学会, Jun. 2014.
74.	堀賢司, 狩山玲子, Keiji Murakami, 光畑律子, 和田耕一郎, 石川亜矢乃, 渡辺豊彦, Yoichiro Miyake and 公文裕巳 : 新規マウス薬効評価系の構築に向けた発光性緑膿菌による尿路バイオフィルム感染症モデルの作製, 第88回日本感染症学会学術講演会第62回日本化学療法学会総会合同学会, Jun. 2014.
75.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Keiji Murakami and Yoichiro Miyake : Extracellular DNA influences pyocyanin production from Pseudomonas aeruginosa, 第87回日本細菌学会総会, Mar. 2014.
76.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao and Yoichiro Miyake : 抗Si-HLP抗体のミトコンドリアATP synthase β subunitに対する交差反応性, 第87回日本細菌学会総会, Mar. 2014.
77.	Keiji Murakami, Nur Asikin, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌臨床分離株における抗菌薬抵抗性と病原性との関連, 第87回日本細菌学会総会, Mar. 2014.
78.	Keiji Murakami : 抗菌薬抵抗性とそのメカニズムについて, 第48回緑膿菌感染症研究会, Jan. 2014.
79.	Tomoko Kimura, Kazumi Ozaki, Hiromichi Yumoto, Keiji Murakami, Chieko Sugawara, Chihiro Shinohara, Emi Takegawa, Yoichiro Miyake, Takashi Matsuo and Fumiaki Kawano : Roles of scrA gene in pathogenicity of Streptococcus mutans, 第6回日本総合歯科学会総会・学術大会, 38, Nov. 2013.
80.	Hideaki Maseda, 上手麻希, Keiji Murakami and Yoichiro Miyake : 環境および臨床由来緑膿菌の特性比較, 第61回日本化学療法学会西日本支部総会, Nov. 2013.
81.	堀賢司, 狩山玲子, 光畑律子, Keiji Murakami, 和田耕一郎, 石井亜矢乃, 渡辺豊彦, Yoichiro Miyake and 公文裕巳 : マウスを用いた緑膿菌性尿路バイオフィルム感染症モデルの作製と各種抗菌薬の治療効果, 第61回日本化学療法学会西日本支部総会, Nov. 2013.
82.	Keiji Murakami, Tsuneko Ono, Natsumi Takamaru, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌臨床分離株による抗菌薬抵抗性と病原因子との関連について, 第61回日本化学療法学会西日本支部総会, Nov. 2013.
83.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami and Yoichiro Miyake : Homologous and heterologous extracellular DNAs affect Pseudomonas aeruginosa to produce more pyocyanin without inducing bacterial growth, 第66回日本細菌学会中国・四国支部総会, Oct. 2013.
84.	Keiji Murakami, Yumi Hoshimo, Katsuhiko Hirota and Yoichiro Miyake : イグサ抽出液によるう蝕および歯周病予防効果の検討, 第55回歯科基礎医学会学術大会, Sep. 2013.
85.	薫廣瀬, 松本紀三江, 笠井千晶 and Keiji Murakami : 大学病院における感染対策について針刺し事故防止への取り組み, 日本歯科衛生学会第8回学術大会, Sep. 2013.
86.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌における抗菌薬抵抗性とpsl遺伝子の役割, 第7回細菌学若手コロッセウム, Aug. 2013. (Keyword) Pseudomonas aeruginosa / 抗菌薬抵抗性 / psl遺伝子
87.	狩山玲子, 堀賢司, 光畑律子, Keiji Murakami, 和田耕一郎, 石井亜矢乃, 渡辺豊彦, Yoichiro Miyake and 公文裕巳 : マウスを用いた緑膿菌性尿路バイオフィルム感染症モデルの作製, 第27回Bacterial Adherence & Biofilm学術集会, Jul. 2013.
88.	Keiji Murakami, Nur Asikin, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌臨床分離株における抗菌薬抵抗性と病原因子との関連について, 第27回Bacterial Agherence & Biofilm学術集会, Jul. 2013.
89.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Effect of extracellular DNA on pyocyanin production from Pseudomonas aeruginosa, 第27回Bacterial Agherence & Biofilm学術集会, Jul. 2013.
90.	Katsuhiko Hirota, Hiromichi Yumoto, Keiji Murakami, Kouji Hirao, Kanako Takahashi, Takashi Matsuo and Yoichiro Miyake : Streptococcus intermediusヒストン様タンパク質のPAMPsとしての解析, 第22回Lancefieldレンサ球菌研究会&第45回レンサ球菌感染症研究会, Jun. 2013.
91.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami and Yoichiro Miyake : The role of extracellular DNA in Pseudomonas aeruginosa and Streptococcus intermedius infection, 第86回日本細菌学会総会, Mar. 2013.
92.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : Effects of theaddition of Clarithromycin on Pseudomonas aeruginosa biofilm formation, 第86回日本細菌学会総会, Mar. 2013.
93.	Katsuhiko Hirota, Hiromichi Yumoto, Nur Asikin, Kouji Hirao, Keiji Murakami and Yoichiro Miyake : Pathogenic roles of Streptococcus intermedius histone-like protein in microbial inflammation, 第86回日本細菌学会総会, Mar. 2013.
94.	白水裕也, 星野佑太, 西田みなみ, 曽宮葉子, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Yoichiro Miyake, Akiko Sakurai, 佐藤雅美, 岡本貴子, 香川葉子 and 畑美智子 : 緑膿菌臨床分離株における抗菌薬耐性のメカニズム, 第36回徳島県医学検査学会, Dec. 2012.
95.	星野佑太, 白水裕也, 西田みなみ, 曽宮葉子, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Yoichiro Miyake, Akiko Sakurai, 佐藤雅美, 岡本貴子, 香川葉子 and 畑美智子 : 緑膿菌臨床分離株における抗菌薬抵抗性と病原因子について, 第36回徳島県医学検査学会, Dec. 2012.
96.	Keiji Murakami, Tsuneko Ono, Natsumi Takamaru, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌における付着及びバイオフィルム形成菌の抗菌薬抵抗性遺伝子のスクリーニング, 第60回日本化学療法学会西日本支部総会, Nov. 2012.
97.	江頭陽子, Keiji Murakami, Katsuhiko Hirota, Hiroki Iga and Yoichiro Miyake : 新規抗菌性界面活性剤の臨床応用を目指した基礎研究, 第65回日本細菌学会中国・四国支部総会, Oct. 2012.
98.	西田みなみ, 曽宮葉子, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : クラリスロマイシンによる緑膿菌RSCVsの誘導について, 第65回日本細菌学会中国・四国支部総会, Oct. 2012.
99.	曽宮葉子, 西田みなみ, Keiji Murakami, Tsuneko Ono and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性に及ぼすpsl遺伝子とc-di-GMPの関与について, 第65回日本細菌学会中国・四国支部総会, Oct. 2012.
100.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami and Yoichiro Miyake : Biological roles of extracellular DNA of Streptococcus intermeius, 第65回日本細菌学会中国・四国支部総会, Oct. 2012.
101.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Role of Extracellular DNA and DNA-binding protein in biofilm formation of Streptococcus intermeius, 第26回Bacterial Adherence & Biofilm学術集会, Jul. 2012.
102.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : 付着及びバイオフィルム形成緑膿菌の抗菌薬抵抗性関連遺伝子の探索, 第26回Bacterial Adherence & Biofilm学術集会, Jul. 2012.
103.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami, Takashi Matsuo and Yoichiro Miyake : Roles of extracellular DNA and DNA-binding protein in cell aggregation, biofilm formation and antibiotic tolerance of Streptococcus intermedius, 第21回Lancefieldレンサ球菌研究会&第44回レンサ球菌感染症研究会合同開催, Jun. 2012.
104.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : クラリスロマイシン添加による緑膿菌への影響, 第60回日本化学療法学会学術集会, Apr. 2012.
105.	Yohko Egashira, Keiji Murakami, Katsuhiko Hirota, Hiroki Iga and Yoichiro Miyake : 新規抗菌性界面活性剤の臨床応用を目指した基礎研究, 四国歯学会第40回例会, Mar. 2012.
106.	Yumi Hoshimo, Keiji Murakami, Katsuhiko Hirota, Daisuke Hinode and Yoichiro Miyake : イグサ粉末の口腔細菌に対する効果, 四国歯学会第40回例会, Mar. 2012.
107.	長尾多美子, 高開登茂子, Momoyo Azuma, Keiji Murakami and Shoji Sakiyama : 大学病院での百日咳疑いアウトブレイクを経験して, 第27回日本環境感染学会総会, Feb. 2012.
108.	Keiji Murakami, Momoyo Azuma, 畑美智子, 長尾多美子, 高開登茂子 and Shoji Sakiyama : 緑膿菌臨床分離株における薬剤耐性とバイオフィルム形成について, 第27回日本環境感染学会総会, Feb. 2012.
109.	Keiji Murakami : 新規抗菌界面活性剤を用いた口腔環境改善方法の検討, 連携機能を活用した口腔からQOL向上を目指す研究平成23年度口腔環境カテゴリー研究報告会, Jan. 2012.
110.	Maki Yamada, Keita Maki, Naoko Okasaka, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase, Yasuki Noma, Yohko Somiya and Minami Nishida : 緑膿菌臨床分離株におけるpel, psl遺伝子の保有と抗菌薬抵抗性との関連について, 第35回徳島県医学検査学会, Dec. 2011.
111.	Keita Maki, Naoko Okasaka, Maki Yamada, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase, Yasuki Noma, Yohko Somiya and Minami Nishida : 緑膿菌臨床分離株におけるバイオフィルム形成能と薬剤感受性について, 第35回徳島県医学検査学会, Dec. 2011.
112.	Naoko Okasaka, Maki Yamada, Keita Maki, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase, Yasuki Noma, Yohko Somiya and Minami Nishida : 徳島大学病院で分離された緑膿菌における薬剤耐性のメカニズムとERIC-PCRの有用性について, 第35回徳島県医学検査学会, Dec. 2011.
113.	Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌における抗菌薬抵抗性関連遺伝子の探索, 第59回日本化学療法学会西日本支部総会, Nov. 2011.
114.	Minami Nishida, Yasuki Noma, Issei Minase, Yohko Somiya, Keiji Murakami, Yoichiro Miyake and Tsuneko Ono : クラリスロマイシンが及ぼす緑膿菌コロニー性状への影響, 第44回中国四国医学検査学会, Nov. 2011.
115.	Yohko Somiya, Yasuki Noma, Issei Minase, Minami Nishida, Keiji Murakami, Yoichiro Miyake and Tsuneko Ono : 緑膿菌psl遺伝子の抗菌薬抵抗性への関与について, 第44回中国四国医学検査学会, Nov. 2011.
116.	Issei Minase, Yasuki Noma, Yohko Somiya, Minami Nishida, Keiji Murakami, Yoichiro Miyake and Tsuneko Ono : バイオフィルム形成菌での抗菌薬抵抗性獲得メカニズムについて, 第44回中国四国医学検査学会, Nov. 2011.
117.	Yasuki Noma, Issei Minase, Yohko Somiya, Minami Nishida, Keiji Murakami, Yoichiro Miyake and Tsuneko Ono : 付着緑膿菌のビアペネム抵抗性関連遺伝子の探索, 第44回中国四国医学検査学会, Nov. 2011.
118.	Yasuki Noma, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 付着緑膿菌における抗菌薬抵抗性に関与する遺伝子の検討, 第64回日本細菌学会中国・四国支部総会, Oct. 2011.
119.	Nur Asikin, Katsuhiko Hirota, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Keiji Murakami and Yoichiro Miyake : The Effect of Extracellular DNA on The Development of Streptococcus intermedius Biofilm, 第64回日本細菌学会中国・四国支部総会, Oct. 2011.
120.	Keiji Murakami : 徳島大学病院における薬剤耐性緑膿菌対策の現状, 第9回徳島県ICTネットワーク研究会, Sep. 2011.
121.	Keiji Murakami and Yoichiro Miyake : バイオフィルム形成緑膿菌における抗菌薬抵抗性関連遺伝子の探索, 第53回歯科基礎医学会学術大会, Sep. 2011.
122.	近藤洋史, Tsuneko Ono, Katsuhiko Hirota, Keiji Murakami, Yoichiro Miyake, Hiromichi Yumoto, Kanako Takahashi, Kouji Hirao and Takashi Matsuo : THP-1細胞のケモカイン産生に及ぼす口腔レンサ球菌ヒストン様DNA結合タンパク質の影響, 第34回徳島県医学検査学会, Dec. 2010.
123.	小寺佑佳, Yohko Somiya, 西田みなみ, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase and Yasuki Noma : 緑膿菌臨床分離株のRSCVの分離と抗菌薬感受性について, 第34回徳島県医学検査学会, Dec. 2010.
124.	西田みなみ, 小寺佑佳, Yohko Somiya, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase and Yasuki Noma : 抗菌薬による緑膿菌RSCVの誘導について, 第34回徳島県医学検査学会, Dec. 2010.
125.	Yohko Somiya, 小寺佑佳, 西田みなみ, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Shizuo Kayama, Katsuhiko Hirota, Yoichiro Miyake, Issei Minase and Yasuki Noma : 緑膿菌におけるc-di-GMPと抗菌薬抵抗性について, 第34回徳島県医学検査学会, Dec. 2010.
126.	Keiji Murakami, Shizuo Kayama, Tsuneko Ono, Katsuhiko Hirota and Yoichiro Miyake : 緑膿菌におけるc-di-GMPと抗菌薬抵抗性との関連について, 第58回日本化学療法学会西日本支部総会, Nov. 2010.
127.	Yumi Hoshimo, Keiji Murakami and Yoichiro Miyake : イグサの口腔細菌に及ぼす影響について, 第63回日本細菌学会中国・四国支部総会, Oct. 2010.
128.	Issei Minase, Shizuo Kayama, Keiji Murakami, Tsuneko Ono and Yoichiro Miyake : 緑膿菌ladS遺伝子の抗菌薬抵抗性への影響について, 第63回日本細菌学会中国・四国支部総会, Oct. 2010.
129.	Katsuhiko Hirota, Hiromichi Yumoto, Yumi Hoshimo, Keiji Murakami, 宮本幸治, Takashi Matsuo and Yoichiro Miyake : 水溶性MPCポリマーの口腔細菌付着抑制効果, Bacterial Adherence &Biofilm学術集会, Jul. 2010.
130.	Keiji Murakami and Yoichiro Miyake : 緑膿菌臨床分離株におけるRSCVsの分離とその性状について, Bacterial Adherence &Biofilm学術集会, Jul. 2010.
131.	Keiji Murakami, Shizuo Kayama, Tsuneko Ono and Yoichiro Miyake : 緑膿菌臨床分離株におけるRSCVの分離と抗菌薬抵抗性について, 第58回日本化学療法学会学術講演会, Jun. 2010.
132.	Shizuo Kayama, Keiji Murakami, Tsuneko Ono, 山本明毅, 谷口友伯, Katsuhiko Hirota, Hideaki Nagamune and Yoichiro Miyake : The role of QS Las-system and sigma factors in antibiotic tolerance in Pseudomonas aeruginosa, 第83回日本細菌学会総会, Mar. 2010.
133.	Tomoko Kimura, Kazumi Ozaki, Hiromichi Yumoto, Keiji Murakami, Shizuo Kayama, 藤坂菊美, Kanako Takahashi and Yoichiro Miyake : Roles and virulence of scrA and htrA genes in Streptococcus mutans, 第83回日本細菌学会総会, Mar. 2010.
134.	Keiji Murakami and Yoichiro Miyake : The mecanism of pel induction in tube biofilm, 第83回日本細菌学会総会, Mar. 2010.
135.	Katsuhiko Hirota, Shizuo Kayama, Keiji Murakami, Hiromichi Yumoto and Yoichiro Miyake : Molecular mechanisms of Intermedilysin induced human ER disfunction, 第83回日本細菌学会総会, Mar. 2010.
136.	高谷亜加里, 福田幸恵, Tsuneko Ono, Chieko Matsuura, Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, 山本明毅 and 谷口友伯 : 緑膿菌臨床分離株におけるwsp関連遺伝子と抗菌薬抵抗性に関する研究, 第33回徳島県医学検査学会, Dec. 2009.
137.	福田幸恵, 高谷亜加里, Tsuneko Ono, Chieko Matsuura, Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Yoichiro Miyake, 山本明毅 and 谷口友伯 : 緑膿菌におけるσ因子関連遺伝子と抗菌薬抵抗性に関する研究, 第33回徳島県医学検査学会, Dec. 2009.
138.	相川文子, Shizuo Kayama, Keiji Murakami, Tsuneko Ono and Yoichiro Miyake : 緑膿菌の抗菌薬抵抗性におけるtcp遺伝子の役割, 四国歯学会第35回例会, Jun. 2009.
139.	Liu Dali, Hiromichi Yumoto, Keiji Murakami, Katsuhiko Hirota, Shizuo Kayama, Takashi Matsuo and Yoichiro Miyake : The essentiality and involvements of Streptococcus intermedius histone-like protein in bacterial viability and normal growth, The 2nd international symposium on "The future direction of oral sciences in the 21st century", Dec. 2007.
140.	Dali LIU, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota and Yoichiro Miyake : Investigation of the toxicity of Streptococcus intermedius histon-like protein in Escherichia coli, 第60回日本細菌学会中国・四国支部総会, Oct. 2007.
141.	LIU Dali, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota and Yoichiro Miyake : Investigation of the essentiality of histone-like protein in Streptococcus intermedius, 第80回日本細菌学会総会, Mar. 2007.
142.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 付着緑膿菌の抗菌薬抵抗性とQuorum sensing機構について, 第80回日本細菌学会総会, Mar. 2007.
143.	Katsuhiko Hirota, LIU Dali, Shizuo Kayama, Keiji Murakami, Hideaki Nagamune, Tsuneko Ono and Yoichiro Miyake : Intermedilysinによる培養ヒト胆管上皮細胞核膜抗原の異所性表出, 第80回日本細菌学会総会, Mar. 2007.
144.	劉大力, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota and Yoichiro Miyake : Investigation of the Essentiality of Histone-Like Protein in Streptococcus intermedius, 第80回日本細菌学会総会, Mar. 2007.
145.	野間保喜, 堀川明日香, 滝本真由美, 玉井利奈, Chieko Matsuura, Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : う蝕原因菌Streptococcus mutansの病原性に関する研究, 第30回徳島県医学検査学会, Dec. 2006.
146.	玉井利奈, 滝本真由美, 野間保喜, 堀川明日香, Chieko Matsuura, Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : 緑膿菌臨床分離株における抗菌薬感受性とバイオフィルム形成に関する研究, 第30回徳島県医学検査学会, Dec. 2006.
147.	滝本真由美, 玉井利奈, 堀川明日香, 野間保喜, Chieko Matsuura, Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : 緑膿菌におけるPQS Quorum Sensingと病原性に関する研究, 第30回徳島県医学検査学会, Dec. 2006.
148.	堀川明日香, 野間保喜, 滝本真由美, 玉井利奈, Chieko Matsuura, Tsuneko Ono, Keiji Murakami and Yoichiro Miyake : 抗菌薬添加によるQuorum Sensing関連遺伝子発現の変動, 第30回徳島県医学検査学会, Dec. 2006.
149.	Keiji Murakami, Shizuo Kayama, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 抗菌薬添加による緑膿菌Quorum Sensing関連遺伝子発現の変化, 第54回日本化学療法学会西日本支部総会, Dec. 2006.
150.	木村智子, Kazumi Ozaki, 藤坂菊美, Keiji Murakami and Yoichiro Miyake : Streptococcus mutansの病原性におけるスクロース輸送系遺伝子の役割について, 第59回日本細菌学会中国・四国支部総会, Oct. 2006.
151.	吉嶋佑佳, Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : 親水性コーティング法による細菌付着抑制効果の検討, 第59回日本細菌学会中国・四国支部総会, Oct. 2006.
152.	LIU Dali, Hiromichi Yumoto, Kanako Takahashi, Keiji Murakami, Katsuhiko Hirota and Yoichiro Miyake : Proinflammatory cytokines are induced in human monocytes in response to exposure to the histone like protein of Streptococcus intermedius, 第59回日本細菌学会中国・四国支部総会, Oct. 2006.
153.	Katsuhiko Hirota, LIU Dali, Shizuo Kayama, Keiji Murakami, Hideaki Nagamune and Yoichiro Miyake : Intermedilysinによるlamin B1の異所性表出, 第59回日本細菌学会中国・四国支部総会, Oct. 2006.
154.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono, Hideaki Nakae and Yoichiro Miyake : 付着緑膿菌の抗菌薬抵抗性とQuorum sensing機構について, Bacterial Adherence & Biofilm 第20回記念学術集会, Jul. 2006.
155.	Keiji Murakami, Shizuo Kayama, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 抗菌薬抵抗性による緑膿菌rpoS遺伝子発現の変化, 第54回日本化学療法学会総会, May 2006.
156.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌Quorum sensingとofloxacin抵抗性について, 第79回日本細菌学会総会, Mar. 2006.
157.	Keiji Murakami, Shizuo Kayama, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 抗菌薬による緑膿菌rpoS遺伝子プロモーター活性への影響, 第79回日本細菌学会総会, Mar. 2006.
158.	Keiji Murakami, 鹿山鎭男, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌Quorum sensingとOfloxacin抵抗性について, 第53回日本化学治療学会西日本支部総会, Dec. 2005.
159.	Keiji Murakami, 鹿山鎭男, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌 tcp 遺伝子が抗菌薬抵抗性に及ぼす影響について, 第58回日本細菌学会中国・四国支部総会, Oct. 2005.
160.	Oheni Susilowati, Katsuhiko Hirota, Dali Liu, Sizuo Kayama, Keiji Murakami, Ken Kikuchi, Kyoichi Totsuka, Hideaki Nagamune and Yoichiro Miyake : The Mechanism of Bile Epithelium Cell Death Under the Stimulation of Streptococcus Intermedius Cytolysin, 第58回日本細菌学会中国・四国支部総会, Oct. 2005.
161.	Keiji Murakami, Shizuo Kayama, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌tcp遺伝子と抗菌薬抵抗性について, 第53回化学療法学会総会, May 2005.
162.	鹿山鎭男, Keiji Murakami, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : P1-202 緑膿菌 lasl, rhll 遺伝子と抗菌薬抵抗性について, 第78回日本細菌学会総会, Apr. 2005.
163.	Keiji Murakami, 鹿山鎭男, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : P1-192 緑膿菌 bta 遺伝子の抗菌薬抵抗性への影響について, 第78回日本細菌学会総会, Apr. 2005.
164.	鹿山鎭男, Keiji Murakami, Darija Viducic, 劉大力, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌 lasl, rhll 遺伝子と抗菌薬抵抗性について, 第52回日本化学治療法学会西日本支部総会, Dec. 2004.
165.	Katsuhiko Hirota, 菊池賢, 劉大力, 鹿山鎭男, Keiji Murakami, Ken Nemoto, Yoichiro Miyake and Tsuneko Ono : 脳腫瘍以来のS.intermedius ILY高産生株に対するカルバベネム系抗菌薬感受性に関する検討, 第52回日本化学治療法学会西日本支部総会, Dec. 2004.
166.	鹿山鎭男, Keiji Murakami, Darija Viducic, 劉大力, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌 Quorum Sensing 機構と抗菌薬抵抗性について, 第57回日本細菌学会中国・四国支部総会, Oct. 2004.
167.	Katsuhiko Hirota, 劉大力, 鹿山鎭男, Keiji Murakami, Ken Nemoto, Akiko Sukeno, Hideaki Nagamune, 菊池賢, 戸塚恭一 and Yoichiro Miyake : 抗Streptococcus intermedius HU型ヒストン様タンパク質抗体のHepG2細胞内ミトコンドリアとの反応性, 第57回日本細菌学会中国・四国支部総会, Oct. 2004.
168.	Katsuhiko Hirota, 劉大力, 鹿山鎭男, Keiji Murakami, Ken Nemoto, Tsuneko Ono and Yoichiro Miyake : Anginosus group streptococci感染症とその続発生, 第2回感染病態研究会シンポジウム「Symbiosis」, Jun. 2004.
169.	Keiji Murakami, Shizuo Kayama, Darija Viducic, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌PAO1株におけるbiapenem抵抗性変異株の分離, 第52回日本化学療法学会総会, Jun. 2004.
170.	榊原恵美子, Hideaki Nagamune, Keiji Murakami, Takuya Maeda, Yoichiro Miyake and Hiroki Kourai : 緑膿菌外膜タンパク質OprRの抗生物質感受性への関与, 日本細菌学会第77回総会, Apr. 2004.
171.	Keiji Murakami, 鹿山鎭男, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 付着緑膿菌の抗菌薬抵抗性変異株の分離, 第77回日本細菌学会総会, Apr. 2004.
172.	Hideaki Nagamune, 榊原恵美子, 田端厚之, Takuya Maeda, Hiroki Kourai, Keiji Murakami and Yoichiro Miyake : 第四アンモニウム塩系消毒剤に対する緑膿菌の耐性化には外膜蛋白質OryRが関与している, 日本防菌防黴学会第30回年次大会, May 2003.
173.	Hideaki Nagamune, Takuya Maeda, Keiji Murakami, Yoichiro Miyake and Hiroki Kourai : 第四アンモニウム塩系消毒剤に対する緑膿菌の耐性化機構:外膜タンパク質QRP01の関与, 日本細菌学会第76回総会, Apr. 2003.
174.	Hiromichi Yumoto, Katsuhiko Hirota, Hideaki Nagamune, Kazuto Ohkura, Keiji Murakami, 山田真義, Hideaki Nakae and Yoichiro Miyake : Streptococcus intermedius hitone-like proteinをコードする遺伝子のクローニングと発現, 第75回日本細菌学会総会, Apr. 2002.
175.	Hiromichi Yumoto, Katsuhiko Hirota, 山田真義, Hideaki Nakae, Keiji Murakami, Yoichiro Miyake and Takashi Matsuo : Streptococcus intermedius histone-like proteinをコードする遺伝子のクローニングと発現, 第44回秋季日本歯周病学会学術大会, Oct. 2001.
176.	山田真義, Hiromichi Yumoto, Keiji Murakami and Hideaki Nakae : 上皮細胞のICAM-1発現誘導におけるEikenella corrodens付着因子の関与について, 第73回日本細菌学会総会, May 2000.

Et cetera, Workshop:

1.	Saho Yamanaka, Rina Murata, Keiji Murakami, Yuka Hiroshima, Hideki Fujii, Akiko Sakurai and Keiko Kataoka : 緑膿菌の抗菌薬抵抗性に関与する二成分制御系について, 第44回徳島県医学検査学会, Dec. 2020.
2.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, 多田彩乃, Tomomi Kuwahara, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
3.	Pahlevi Reza Muhammad, Keiji Murakami, Yuta Kita, Rina Murata, Yuka Hiroshima and Hideki Fujii : Screening for the genes influenced by AIA-1 in Pseudomonas aeruginosa, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
4.	AKIZUKI Minato, Keiji Murakami, Yuka Hiroshima, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングにおけるTi表面への歯周病原菌付着抑制効果の検討, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
5.	Yuta Kita, Pahlevi Reza Muhammad, Rina Murata, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : バイオフィルム形成緑膿菌におけるPA2384遺伝子の役割について, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
6.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
7.	喜田悠太, Pahlevi Reza Muhammad, Keiji Murakami, Yuka Hiroshima and Hideki Fujii : 緑膿菌PA2384遺伝子の抗菌薬抵抗性への関与, 四国歯学会第55回例会, Sep. 2019.
8.	鹿庭美奈子, 喜田悠太, Keiji Murakami, Yuka Hiroshima, Takashi Amoh and Hideki Fujii : BNCのインフルエンザ感受性細胞への接着に関与する温度条件, 四国歯学会第54回例会, Mar. 2019.
9.	Keiji Murakami, 村田梨菜, Takashi Amoh, Keiko Kataoka and Hideki Fujii : 緑膿菌臨床分離株における抗菌薬抵抗性と抗酸化能との関連について, 第53回緑膿菌感染症研究会プログラム, Mar. 2019.
10.	Natsumi Fujiwara, Miki Tsurukuma, Kaya Yoshida, Keiji Murakami, Kazumi Ozaki, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングによる義歯用レジンのカンジダ付着抑制効果, 2018 Bioscience retreat in Awaji, Nov. 2018.
11.	Takashi Amoh, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Katsuhiko Hirota, Yoichiro Miyake and Hideki Fujii : 幼児口腔内から検出された多剤耐性レンサ球菌について, 第71回日本細菌学会中国，四国支部総会, Oct. 2018.
12.	Keiji Murakami, 狩山玲子, 公文裕巳 and Yoichiro Miyake : 緑膿菌Autoinducer Analogがマクロライドの抗菌作用に及ぼす影響について, 第52回緑膿菌感染症研究会講演記録, Vol.52, 67, Oct. 2018.
13.	Mizuki Abe, Narumi Senoh, Keiji Murakami, Takashi Amoh, Hideki Fujii, 佐藤雅美, 笹田倫子, 菅崎幹樹, 森本悠里, 平尾早紀, Akiko Sakurai and Keiko Kataoka : オートインデューサーアナログ(AIA)の緑膿菌に及ぼす影響, 第41回徳島県医学検査学会, Dec. 2017.
14.	Shinichi Fujie, Shoto Ogawa, Keiji Murakami, Takashi Amoh, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 呼吸器由来緑膿菌における病原性と抗菌薬抵抗性との関連について, 第40回徳島県医学検査学会, Dec. 2016.
15.	Keiko Kataoka, 南亜利沙, Keiji Murakami, Yoichiro Miyake, 畑美智子, 佐藤雅美, 岡本貴子, 香川葉子, 菅崎幹樹 and Momoyo Azuma : 本院で分離されたMRSAの分類とその特徴, 徳島県医学検査学会, Dec. 2013.
16.	Keiko Kataoka, 堀口なつみ, Keiji Murakami, Yoichiro Miyake, 畑美智子, 佐藤雅美, 岡本貴子, 香川葉子, 菅崎幹樹 and Momoyo Azuma : 「緑膿菌臨床分離株における抗菌薬抵抗性について」, 徳島県医学検査学会, Dec. 2013.
17.	Keiji Murakami, Momoyo Azuma, 畑美智子, 長尾多美子, 鈴木麗子, Yoichiro Miyake and Shoji Sakiyama : 徳島大学病院におけるパルスフィールドゲル電気泳動法(PFGE)によるMRSAの分子疫学調査, 第4回MRSAフォーラム, Jul. 2013.
18.	Keiji Murakami : 徳島大学病院で分離されたMRSAのパルスフィールドゲル電気泳動法(PFGE)による分子疫学解析, 第11回徳島県ICTネットワーク研究会, Jul. 2013.
19.	Keiji Murakami : 徳島大学病院における耐性菌の分離状況とその対策について, 感染防止対策加算連携病院第2回カンファレンス・徳島大学病院平成24年度第1回感染対策研修会, Jun. 2012.
20.	Keiji Murakami : 徳島大学病院における緑膿菌院内感染対策について, 徳島大学病院臨床検査技術部門勉強会(5月度), May 2012.
21.	Keiji Murakami : 徳島大学病院感染対策歯科部門講習会, 徳島大学病院感染対策歯科部門講習会, May 2012.
22.	Keiji Murakami : 徳島大学病院感染対策歯科部門講習会, 徳島大学病院感染対策歯科部門講習会, Apr. 2011.
23.	Keiji Murakami : 細菌学的に見た院内感染対策の考え方, 徳島県歯科医師会主催「医療安全管理体制講演会」, Jul. 2010.
24.	Katsuhiko Hirota, 米山武義, 栗原正紀, 宮本寛, 坂本まゆみ, Keiji Murakami and Yoichiro Miyake : 摂食嚥下障害のある脳血管障害患者と緑膿菌, はち・まる・にい・まる 8020, No.7, 108-109, Jan. 2008.
25.	Shizuo Kayama, Keiji Murakami, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 付着緑膿菌の抗菌薬抵抗性とQuorum sensing機構について, Bacterial Adherence & Biofilm, Vol.20, 110-115, Jul. 2006.
26.	Keiji Murakami and Yoichiro Miyake : バイオフィルムにおける遺伝子発現とクオラムセンシング, Dental Outlook, Vol.100, No.3, 612-613, Sep. 2002.
27.	Katsuhiko Hirota, Hiromichi Yumoto, 村田広美, Viducic Darijia, 谷口和子, Keiji Murakami, Ken Nemoto, Tsuneko Ono and Yoichiro Miyake : Staphyrococcus aureusにおけるhistone-like proteinの存在と構造解析, 第46回ブドウ球菌研究会, Sep. 2001.
28.	谷口和子, Keiji Murakami, Tsuneko Ono, Katsuhiko Hirota, Ken Nemoto and Yoichiro Miyake : 緑膿菌におけるBIPM抵抗性変異株の作成, Bacterial Adherence & Biofilm, Vol.15, 22-26, Jan. 2001.
29.	Keiji Murakami, 谷口和子, Darija Viducic, Ken Nemoto, Katsuhiko Hirota, Tsuneko Ono and Yoichiro Miyake : 緑膿菌抗菌薬抵抗性におけるストレス反応の影響, Bacterial Adherence & Biofilm, Vol.15, 27-30, Jan. 2001.
30.	Keiji Murakami, Tsuneko Ono, 谷口和子, Takashi Matsuo and Yoichiro Miyake : 付着緑膿菌における抗菌薬抵抗性変異株の分離とその性状, Bacterial Adherence & Biofilm, Vol.13, 23-25, Jan. 1999.

Patent:

1.	Hideki Fujii and Keiji Murakami : 殺菌剤及び殺菌方法, (Nov. 2018), .

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

腸内細菌叢の改善による反復性膀胱炎の新たな予防法と治療法の開発 (Project/Area Number: 22K09473 )
緑膿菌における病原性、抗菌薬抵抗性のトレードオフ機構の解明 (Project/Area Number: 22K08613 )
バイオナノカプセルを用いた高齢者オーラルケアの基礎研究 (Project/Area Number: 20K09941 )
Roles of Fusobacterium nucleatum in Systemic Inflammations by Cancer Chemotherapy (Project/Area Number: 19K08839 )
２成分制御系を中心としたバイオフィルム形成菌における抗菌薬抵抗性メカニズムの解明 (Project/Area Number: 18K09535 )
A study on oxidative stress as bactericidal mechanism of antibacterial agents by metabolome analysis (Project/Area Number: 16K11446 )
The mechanisms of antibiotic tolerance focusing on intracellular signaling substance c-di-GMP. (Project/Area Number: 26462787 )
Development of oral probiotics using multi-bacteria (Project/Area Number: 25670886 )
Analyses of mechanism of action of a quorum sensing inhibitor by using real-time imaging system (Project/Area Number: 25461512 )
Molecular characterization of the pathogenic factors of oral streptococci involved in autoimmune disease (Project/Area Number: 24592833 )
Development of novel methods for identifying antibiofilm agents against multidrug-resistant Acinetobacter baumannii (Project/Area Number: 23659759 )
The screening for antibiotic tolerance related genes in peg-biofilm cells of Pseudomonas aeruginosa (Project/Area Number: 22592040 )
Regulatory Network for Expression of Antibiotic Tolerance in Pseudomonas aeruginosa (Project/Area Number: 21590627 )
The effect of intermedilysin on human bile duct cells (Project/Area Number: 18592003 )
Molecular analysis of anteliotic-tolerance and stress response in adherent bacteria (Project/Area Number: 17591914 )
付着緑膿菌による抗菌薬抵抗性メカニズムについて (Project/Area Number: 16791109 )
The characterization of DNA-binding protein from Streptococcus intermediusand elucidate its virulence mechanism (Project/Area Number: 14571788 )
A study Of ora| streptococcal histone-like protein and virulence mechanism (Project/Area Number: 12671827 )
Search by Researcher Number (10335804)