| Project/Area Number |
16K09926
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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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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
出原 賢治 佐賀大学, 医学部, 教授 (00270463)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ペリオスチン / マスト細胞 / 脱顆粒 / 細胞外マトリックス / アレルギー反応 / インテグリン / 細胞外マトリクス / アレルギー炎症 / アレルギー / シグナル伝達 |
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| Outline of Final Research Achievements |
Previous studies have suggested that periostin, a matricellular protein, plays an important role in the development of allergic inflammation by interacting with its receptor αV integrin of fibroblasts and epithelial cells. However, the functions of periostin on immune cells are unclear. Mast cells are central effector cells of allergic reactions. Thus, we investigated whether periostin has the potential to induce or modulate mast cell activation via αV integrin. In this study, we demonstrated that periostin, immobilized on a culture plate, augments IgE-mediated degranulation response and LTC4 production by adhering with murine mast cells. The amplifying effect of periostin on degranulation required Mg2+. However, CP4715, an αV integrin inhibitor, had no suppressive effects on adhesion and enhancement of degranulation, which suggests that other integrins are involved in periostin-mediated enhancement of mast cell activation as receptor.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では，IgE受容体を介したマスト細胞の活性化の一つである脱顆粒応答がペリオスチンとの相互作用によって増強されることを見出した。アトピーなどの病的な炎症を起こしている組織では，ペリオスチンの沈着が顕著であり，炎症の現場ではペリオスチンがマスト細胞の活性化をさらに亢進させていると考えられる。本研究の成果により，ペリオスチンとマスト細胞の接着機構が，増大した炎症反応の新たな分子標的と成り得ることが明らかとなった。
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