| Project/Area Number |
16K19439
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | SLPI / インフルエンザ / Reactive Oxygen Species / 幹細胞 / インフルンザ |
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| Outline of Final Research Achievements |
We previously reported two important point for the relationship about influenza pneumonia and lung stem cell. First, bronchiolar progenitor cell is more sensitive for influenza virus than other lung cells, Second,secretory leukocyte protease inhibitor (SLP), which is antiprotenase inhibitor, is important for club cell differentation from bronchiolar progenitor cell. From these things, we hypothesis that SLPI is important for influenza pneumonia.First we evaluated that survival rate and lung inflammation of influenza pneumonia model in SLPI KO and WT mice. Lung inflammation but not survival rate is meekly increased increased in SLPI KO mice than WT. We next evaluated that lung macrophage differentiation by using M/M2 method. In SLPI KO mice, M1/M2 differentiation is more activated than WT mice. Last, We evaluated the pathology of activating M1 macrophage. In SLPI KO mice, the level of inflammation cytokines such as TNF α and IFNγ is more unregulated than WT mice.
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