| Project/Area Number |
23791131
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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 |
Infectious disease medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | インフルエンザウイルス / 気管支喘息 / 肺傷害 / 線維化 / エラスターゼ / 喘息 / コラーゲン / II型肺胞上皮 / インフルエンザ / 急性呼吸不全 |
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| Research Abstract |
Influenza virus is the reason of acute exacerbation bronchial asthma. However, it was lack of understanding for this mechanism. First, we have utilized mouse models of bronchial asthma induced by ovalbumin to experimentally examine a possible aggregation between influenza virus and asthma. We could not find any difference of clinical outcome, accumulation of inflammatory cells and Th1/Th2 related cytokines between normal and asthma mouse after influenza virus infection. We, next, examined whether tissue remodeling was observed after severe inflammation by influenza virus infection. Mice were inoculated non-lethal dose of influenza virus, histopathological analysis presented bronchiectasis and peribronchial collagen diposition and collagen level in the lung was significantly elevated compared to normal mice at the day 35 post-infection. This model could be a novel experimental tool for approaching the pathogenic mechanism of bronchial remodeling after sever inflammation.
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