| Project/Area Number |
24790810
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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 | Kobe University |
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Principal Investigator |
NAGANO Tatsuya 神戸大学, 医学(系)研究科(研究院), 研究員 (80624684)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ホスホリパーゼCイプシロン / 喘息 / Th2細胞 / マウス / 卵白アルブミン / ホスホリパーゼCepsilon / ヘルパーT細胞2型 / 細胞内シグナリング / 国際情報交換 |
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| Research Abstract |
Phospholipase Cepsilon (PLCepsilon) is an effector of Ras and Rap small GTPases and is highly expressed in non-immune cells such as epithelial cells. PLCepsilon has been shown to play a role in inflammation in the skin. This study aimed to elucidate its role in the respiratory immune system by employing an allergic asthma model using the mutant mice where PLCepsilon is enzymatically inactive. In the elicitation stage of the asthma, PLCepsilon deficient mice exhibited substantially attenuated airway hyper-responsiveness accompanied by reduced airway inflammation with a decrease in the Th2 cytokine levels. This attenuated airway inflammation seems to be caused by inhibition of cytokine production from the bronchial epithelial cells as demonstrated by immunohistochemical studies of the allergen-sensitized PLCepsilon deficient mice upon allergen challenge. These results demonstrate an important role of PLCepsilon in the respiratory immune system, at least that mediated by Th2 cells.
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