| Project/Area Number |
24591154
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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 | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOHYAMA Tadashi 帝京大学, 医学部, 教授 (00302703)
YAMAMOTO Hiroshi 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), その他部局等, 研究員 (10361487)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 抗菌ペプチド / ATP / 急性肺損傷 / defensin / 敗血症 |
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| Outline of Final Research Achievements |
The past investigations of the genetic polymorphism suggested that the increase of the antimicrobial peptide, defensin, ex. hBD-3 and mBD-14 augment inflammation in various pulmonary diseases. In this investigation, the acute lung injury model of mBD-14-deficient mice showed that inflammatory responses were reduced in the mBD-14-deficient mice. hBD-3 induced the increase in ATP concentration in airway cells, and the cytotoxicity of hBD-3 was inhibited by the antagonists of ATP. Furthermore, the injection of ATP antagonists reduced the inflammatory responses in acute lung injury model. However, we could not indicate the increase in mBD-14 expression in this model, which suggested that mBD-14 would not directly damage lung cells in vivo.
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