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2020 Fiscal Year Final Research Report

Investigation of the pathogenesis of intractable inflammatory bowel diseases: the role of innate lymphoid cells in the mucosal immune system

Research Project

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Project/Area Number 17H04159
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Gastroenterology
Research InstitutionOsaka University

Principal Investigator

Iijima Hideki  大阪大学, 医学系研究科, 准教授 (90444520)

Co-Investigator(Kenkyū-buntansha) 井上 隆弘  大阪大学, 共創機構, 准教授 (30648184)
新崎 信一郎  大阪大学, 医学系研究科, 講師 (60546860)
林 義人  大阪大学, 医学系研究科, 助教 (80647123)
辻井 芳樹  大阪大学, 医学系研究科, 寄附講座助教 (80795170)
川井 翔一朗  大阪大学, 医学部附属病院, 医員 (10771321)
Project Period (FY) 2017-04-01 – 2021-03-31
Keywords腸管粘膜遊走 / 非ステロイド性消炎鎮痛薬 / 小腸粘膜バリア / 小腸粘膜傷害 / 腸内細菌
Outline of Final Research Achievements

A chemokine receptor, CCR7 is involved in immune-related cell motility of the mucosal immune system. Mucosal injury of the small intestine caused by intraperitoneal administration of a non-steroidal anti-inflammatory drug (NSAID), indomethacin, was significantly worse in chemokine receptor CCR7-deficient mice than in wild-type mice. The mucosal injury was related to the expression of interleukin (IL)-22 binding protein (IL-22BP) produced by dendritic cells which inhibits the mucosal barrier function by IL-22. This study revealed that cell migration in the gastrointestinal mucosal immune system plays an important role in preventing gastrointestinal mucosal injury caused by NSAID.

Free Research Field

消化器内科学

Academic Significance and Societal Importance of the Research Achievements

非ステロイド性消炎鎮痛剤(NSAID)の使用に伴う腸管粘膜傷害における粘膜免疫系の役割についての詳細は不明であったが、本研究によりCCR7というホーミングレセプターの非存在下では腸管粘膜バリアの恒常性維持に関わるIL-22を阻害するCD103陽性樹状細胞が多く存在し、腸管炎症を増悪させることを世界で初めて示した。本研究は、NSAIDによる消化管粘膜傷害の予防法を確立する上で重要であり、新規治療法の開発の端緒となり、安全な疼痛コントロール法の確立に寄与することが期待される。

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Published: 2022-01-27  

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