A Research of Epithelium-Immune Interaction during Mucosal Repair in Inflammatory Bowel Disease
| Project/Area Number |
17KK0166
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| Research Category |
Fund for the Promotion of Joint International Research (Fostering Joint International Research)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | University of Toyama |
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Principal Investigator |
Hayashi Shusaku 富山大学, 学術研究部薬学・和漢系, 助教 (10548217)
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| Project Period (FY) |
2018 – 2022
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥13,910,000 (Direct Cost: ¥10,700,000、Indirect Cost: ¥3,210,000)
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| Keywords | 粘膜治癒 / 大腸上皮細胞 / 遊走 / BLT1 / オルガノイド / 腸管上皮細胞 / GPCR / 炎症性腸疾患 / 大腸オルガノイド / CD11c陽性細胞 / 腸管粘膜修復 / 腸管上皮 / CMKLR1 / 大腸上皮オルガノイド / 腸管粘膜バリア / 腸管マクロファージ / 上皮・免疫連関 / IBD |
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| Outline of Final Research Achievements |
Damaged colonic mucosa by inflammation is regenerated through mucosal repair centered on crosstalk between epithelial cells and immune cells, however mucosal repair is a complex event and details are still unknown. Therefore, in order to clarify mechanisms of mucosal repair, we conducted an international joint research with the University of Michigan School of Medicine. As a result, we discovered a new mechanism of mucosal repair regulated by leukotriene B4 and its receptor BLT1, which have been recognized as inflammatory mediators. In other words, we demonstrated for the first time at the cellular and biological levels that colonic epithelial cells express BLT1, its expression is elevated under inflammation, and that BLT1 in colonic epithelial cells plays a role in promoting mucosal repair after injury.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、大腸上皮細胞に発現するBLT1によって調節される大腸粘膜での粘膜治癒の新たなメカニズムを示した。粘膜治癒の調節には、炎症反応と修復反応のバランスが重要である。従来、もっぱら炎症を惹起するとされてきたロイコトリエンB4-BLT1経路が粘膜治癒を促すことを証明した本研究成果は、複雑な粘膜治癒イベントの解明に貢献するもので、粘膜治癒の達成が再燃予防の鍵となる炎症性腸疾患に対する有用な新規コンセプトを持つ治療戦略の創出への応用が期待される。
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Report
(6 results)
Research Products
(10 results)
