| Project/Area Number |
24591132
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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 |
Respiratory organ internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUKUYAMA Satoru 九州大学, 大学病院, 助教 (50380530)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | COPD / 気管支喘息 / B7-H1 / PD-L1 / 低分子化合物 / ウィルス感染 / 2本鎖RNA / poly IC / virus / PI3 kinase delta / mouse / 国際情報交換 |
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| Outline of Final Research Achievements |
Airway viral infection leads to exacerbation of COPD and asthma. B7-H1(PD-L1) is induced on virus-infected cells and works as an inhibitor of anti-viral defence. The elucidation of induction mechanisms is expected to dampen persistent infection. In an experimental model in which B7-H1 is induced by a synthetic analogue of viral double-stranded RNA, poly IC, or respiratory syncytial virus on human airway epithelial cells, we showed that virus-related induction of B7-H1 depends on the activation of PI3 kinase, a representative kinase in cell proliferation and maintaining of cell survival. Additionally, we have developped in vivo experimental model that airway inflammation with B7-H1 upregulation is induced by intra-tracheal administration of poly IC in mice. Treatment of mice with a PI3 kinase inhibitor tended to attenuate the poly IC-induced upregulation of B7-H1. These results suggest that PI3 kinase may be a therapeutic target of virus-induced pathgenesis of chronic airway diseases.
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