Tokushima University / Educator and Researcher Directory --- Imakura, Takeshi

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Tokushima University ⟩ University Hospital ⟩ Clinical Division ⟩ Department of Internal Medicine ⟩ Respiratory and Rheumatology Medicine ⟩

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Research

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Academic Paper (Judged Full Paper):

1.	Haruka Nishimura, Hiroshi Kawano, Seidai Satou, Takeshi Imakura, Yuya Yamashita, Kojin Murakami, Keiko Haji, Hiroki Bando, Nobuhito Naito, Kozo Kagawa, Yuta Isomura, Kazuya Koyama, Hirohisa Ogawa, Yoshihiro Nishimura and Yasuhiko Nishioka : Analysis of the anti-fibrotic potential of a JAK inhibitor in a bleomycin-induced pulmonary fibrosis model, The Journal of Medical Investigation : JMI, 72, 3, 298-307, 2025. (Summary) Interstitial lung disease (ILD) associated with connective tissue diseases (CTD-ILD) remains to be a major cause of mortality. Different from idiopathic form, CTD-ILD involves more immune dysregulation along with aberrant fibroblast activation. Therefore, therapy targeting both profibrotic and proinflammatory molecules could be ideal for CTD-ILD. Janus kinase (JAK) is a family of intracellular, non-receptor tyrosine kinases that transduce cytokine-mediated signals. The purpose of this study is to reveal the anti-fibrotic potential of JAK inhibitors (JAKis). The anti-fibrotic effect of a JAKi with a particular focus on baricitinib was examined using a human lung fibroblast cell line and a bleomycin (BLM)-induced pulmonary fibrosis model in mice. Baricitinib, a selective JAK1, 2 inhibitor suppressed transforming growth factor-β (TGF-β)-induced phosphorylation of JAK2 in human lung fibroblasts. Baricitinib also strongly suppressed the TGF-β-induced collagen1 and α-smooth muscle actin (α-SMA) expression in fibroblasts. Moreover, baricitinib ameliorated lung fibrosis in BLM-treated mice, particularly when administered in the late phase. The number of α-SMA or collagen triple helix repeat containing 1 (CTHRC1) positive fibroblasts in BLM-treated lungs was reduced by administration of baricitinib. Our data suggest that baricitinib may improve pulmonary fibrosis by directly inhibiting fibroblast activation via JAK2 blockade. J. Med. Invest. 72 : 298-307, August, 2025. (Keyword) baricitinib / Connective tissue disease / Janus kinase Inhibitor / Pulmonary fibrosis / Transforming growth factor-β (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.72.298 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 41183930 ● Summary page in Scopus @ Elsevier: 2-s2.0-105020773260 (DOI: 10.2152/jmi.72.298, PubMed: 41183930, Elsevier: Scopus)
2.	Yuki Tsukazaki, Hirokazu Ogino, Yoshio Okano, Soji Kakiuchi, Shoko Harada, Yuko Toyoda, Yugo Matsumura, Seiya Ichihara, Takeshi Imakura, Rikako Matsumoto, Ryohiko Ozaki, Ei Ogawa, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Hiroto Yoneda, Masaki Hanibuchi, Kayoko Hase, Eiji Takeuchi, Takashi Haku and Yasuhiko Nishioka : Granulocyte colony-stimulating factor has the potential to attenuate the therapeutic efficacy of chemo-immunotherapy for extensive-stage small-cell lung cancer, International Journal of Clinical Oncology, 29, 10, 1451-1460, 2024. (Summary) Granulocyte colony-stimulating factor (G-CSF) has the potential to attenuate the anti-tumor immune responses of T-cells by increasing immune suppressive neutrophils and myeloid-derived suppressor cells. However, the clinical impact of G-CSF on the efficacy of immunotherapy remains unknown. This multi-center retrospective analysis evaluated the impact of G-CSF in patients with extensive-stage small-cell lung cancer (ES-SCLC) treated with chemo-immunotherapy. We analyzed 65 patients with ES-SCLC who completed four cycles of induction chemo-immunotherapy and evaluated the effects of G-CSF on progression-free survival (PFS), overall survival (OS), and a durable response to immunotherapy (defined as PFS 12 months). Fifty patients (76.9%) received 1 dose of G-CSF. The PFS of the patients with G-CSF was poorer than that of the patients without G-CSF (median PFS 8.3 vs. 4.9 months, p = 0.009). The OS of the patients with G-CSF tended to be shorter, but not statistically significant, than that of the patients without G-CSF (median OS 24.3 vs. 16.4 months, p = 0.137). In the multivariate analysis, G-CSF administration was associated with poorer PFS (hazard ratio 2.78, 95% CI 1.36-5.69, p = 0.005) and was identified as a determinant of a durable response (odds ratio 0.18, 95% CI 0.04-0.80, p = 0.024). These results were consistent with other definitions of G-CSF administration (administration of 1 dose of pegfilgrastim, or either 5 doses of filgrastim or 1 dose of pegfilgrastim). G-CSF has the potential to attenuate the efficacy of immunotherapy; therefore, the indication for G-CSF during chemo-immunotherapy should be carefully considered for ES-SCLC. (Keyword) Chemo-immunotherapy / Extensive-stage small-cell lung cancer / Granulocyte colony-stimulating factor (Link to Publication Site) ● Publication site (DOI): 10.1007/s10147-024-02586-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39009900 ● Summary page in Scopus @ Elsevier: 2-s2.0-85198503607 (DOI: 10.1007/s10147-024-02586-0, PubMed: 39009900, Elsevier: Scopus)

Proceeding of International Conference:

1.	Yuki Tsukazaki, Hirokazu Ogino, Yoshio Okano, Soji Kakiuchi, Shoko Harada, Yuko Toyoda, Yugo Matsumura, Seiya Ichihara, Takeshi Imakura, Rikako Matsumoto, Ryohiko Ozaki, Ei Ogawa, Yutaka Morita, Atsushi Mitsuhashi, Yohei Yabuki, Hiroto Yoneda, Masaki Hanibuchi, Kayoko Hase, Eiji Takeuchi, Takashi Haku and Yasuhiko Nishioka : The Conflicting Impacts of G-CSF on the Therapeutic Efficacy of Chemoimmunotherapy for Extensive Stage Small Cell Lung Cancer, 2024 World Conference on Lung Cancer, San Diego, Sep. 2024.

Proceeding of Domestic Conference:

1.	Tatsuya Kajimoto, Hiroshi Kawano, Takeshi Imakura, Yuya Yamashita, Nobuhito Naito, Hirokazu Ogino, Seidai Satou and Yasuhiko Nishioka : 水疱性類天疱瘡を合併したIgG4関連疾患の1例, 第36回日本リウマチ学会中国・四国支部学術集会, Oct. 2025.
2.	Hiroshi Kawano, Takeshi Imakura, Yuya Yamashita, Nobuhito Naito, Hirokazu Ogino, Seidai Satou and Yasuhiko Nishioka : TAFRO症候群の2例, 第36回日本リウマチ学会中国・四国支部学術集会, Oct. 2025.
3.	Takeshi Imakura, Kazuya Koyama, Seidai Satou, Yuta Isomura, Ryoko Suzue, Kojin Murakami, Yuya Yamashita, Nobuhito Naito, Keiko Haji, Hiroki Bando, Hiroshi Kawano and Yasuhiko Nishioka : 関節リウマチ関連間質性肺疾患における血清ペントラキシン2 の診断的有用性の検討, 第5回日本びまん性肺疾患研究会, Sep. 2025.
4.	Keiko Haji, 西村春佳, Hiroshi Kawano, Seidai Satou, Takeshi Imakura, Yuya Yamashita, Hiroki Bando, Nobuhito Naito, Hirohisa Ogawa and Yasuhiko Nishioka : TGF-β/JAK2 経路を標的としたJAK 阻害薬の肺線維症抑制効果の検討, 第5回日本びまん性肺疾患研究会, Sep. 2025.
5.	MIYAMOTO Kenya, Masaki Hanibuchi, Yuya Yamashita, Yutaka Morita, Takeshi Imakura, Hirokazu Ogino, Hiroshi Kawano, Seidai Satou and Yasuhiko Nishioka : 気管支鏡検査後の呼吸器感染症に対する予測因子の解析と予防的抗菌薬投与の意義, 第271回徳島医学会学術集会, Jul. 2025.

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

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