| Project/Area Number |
18K06802
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 47060:Clinical pharmacy-related
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| Research Institution | Suzuka University of Medical Science |
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Principal Investigator |
Ooi Kazuya 鈴鹿医療科学大学, 薬学部, 教授 (40406369)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 乾燥皮膚 / 皮膚バリア機能 / マスト細胞 / コラーゲン / TSLP / 皮膚免疫 / 関節炎 / 非ステロイド性抗炎症薬 / 炎症 |
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| Outline of Final Research Achievements |
In arthritic mice, mast cell proliferation was inhibited by the c-kit antibody, and the effect on dry skin was confirmed. In addition, the decrease in collagen in the skin and the increase in the number of mast cells were suppressed. Furthermore, factors such as TSLP, neutrophils, and active oxygen were involved. Next, we examined Th2 cells and Th17 cells that differentiated by stimulation of dendritic cells. Dry skin improved after Th2 and Th17 inhibitors. Arthritis mice treated with Th2 inhibitors had lower IL-6 and TNF-α than non-treated arthritic mice, and Th17 inhibitor administration reduced the number of mast cells in the skin. It was suggested that Th2 cells and Th17 cells induce dry skin expression by different mechanisms.
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| Academic Significance and Societal Importance of the Research Achievements |
関節リウマチ患者において症例報告が散見される乾燥皮膚に着目した。関節炎においてマスト細胞が乾燥皮膚の誘導に関わる点については、すでに報告した消化器疾患モデルマウスでの現象と類似するが、TSLPやグルココルチコイド、樹状細胞などが関わる点については、関節炎特有の乾燥皮膚の誘導メカニズムであると考えられた。次に非ステロイド性抗炎症薬を関節炎マウスに投与することで、関節炎から誘導される乾燥皮膚が抑制されるかについて検討している。これらの知見も踏まえて、疾患によって乾燥皮膚の誘導メカニズムが異なる可能性が提示され、疾患ごとに適正な乾燥皮膚対策を講じることが可能な科学的根拠となるものと確信している。
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