| Project/Area Number |
25461518
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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 |
Infectious disease medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | IL-13 / TGFβ / 炎症性サイトカイン / Th1関連応答 / インフラマソーム / オリゴ多糖体 / 静脈感染 / IL-1β / 樹状細胞 / リンパ節 / ゼプシス / 初期抗体 / TNFα / バイオマーカー / 炎症蛋白 / IgM / 自然抗体 / 血流感染 / 抗炎症作用 |
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| Outline of Final Research Achievements |
To clarify a role of IL-13 in early host resistance to streprococci, and C. albicans, murine airway and intravenous infection models were used. A low dose administration of these pathogens induced natural and early acquired IgM protection, while high dose administration promoted rapid local inflammatory responses to lung and kidney as infected local organs. In high dose administration, IL-13 suppressed IL-1β, CXCL２ and TNFα that may be detrimental to host for pathogen elimination. However late IL-17A was dependent on TGFβ synthesis, which is also strictly dependent on IL-13. This anti-inflammatory role of IL-13 may be promoted with a chitin-oligomer as an oligosaccharides. Oligosaccharide-IL-13-TGFβ cascades may become more critical for a recovery from sepsis as it suppresses an excessive inflammasome activation during a fatal septic condition. The in vivo finding above was supported in vitro tests of bone-marrow derived cells with additional recombinant (r)IL-13, and rTGFβ.
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