| Project/Area Number |
25860825
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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 |
Aoyagi Tetsuji 東北大学, 医学(系)研究科(研究院), 講師 (50581609)
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 急性肺傷害 / 繊維化 / Influenza virus / Lipopolysaccharides / Claudin / Microparticles / Lipopolysaccharide / インフルエンザウイルス / Tight-junction / 肺傷害 / 肺線維化 / Elastase |
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| Outline of Final Research Achievements |
The clinical course and pathophysiological feature of ARDS are characterized as three phases: acute exduative, proliferative and fibrotic. We investigated the role of claudins, a family of proteins in the components of the tight junction, in acute and fibrotic phase of lung injury. We induced nonviral ARDS by alpha-galactosylceramide(GalCer) and LPS and viral ARDS by influenza virus infection. Claudin-5 and -18 are expressed in naive lungs. In both ARDS model, expression of claudin-4 was elevated and claudin-18 mRNA decreased in acute phases of lung injury. Claudin-4 was expressed in not only epithelial cells but leukocytes recruited into the lungs. Micorparticles in BAL fluid after influenza virus infection was observed. Influenza virus induced MPs have a potential to induced the cytokines and chemokines in alveolar machrophasge. These results indicated that claudins may be involved in the pathogenesis of acute phase of lung injury.
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