| Project/Area Number |
23591113
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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 | Chiba University |
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Principal Investigator |
HIROSE KOICHI 千葉大学, 医学(系)研究科(研究院), 准教授 (90400887)
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| Co-Investigator(Kenkyū-buntansha) |
TAKATORI Hiroaki 千葉大学, 医学部附属病院, 助教 (30568225)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAJIMA Hiroshi 千葉大学, 大学院医学研究院, 教授 (00322024)
SUTO Akira 千葉大学, 大学院医学研究院, 特任准教授 (50447306)
IKEDA Kei 千葉大学, 医学部附属病院, 助教 (10456014)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | IL-25 / Th9細胞 / 肺動脈周囲炎 / 血管リモデリング / 気道上皮細胞 / アレルギー性炎症 / 肺動脈リモデリング / 平滑筋増生 / 気管支喘息 / Th2細胞 / ハウスダスト / 難治性喘息 / Churg-Straus症候群 |
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| Research Abstract |
Recent studies have shown that prplonged Th2-type immune inflammation in the lung induces pulmonary arterial remodeling. However, roles of IL-25, which promotes Th2-type inflammation, in the development of pulmonary arterial remodeling remain unknown. In this study, we evaluated the role of IL-25 in the development of pulmonary arterial remodeling. Repeated OVA inhalation induced pulmonary arterial wall thickening and the expression of IL-25 and RELMa mRNA in the lung in OVA-sensitized mice. Injection of neutralizing anti-IL-25 antibody inhibited OVA-induced pulmonary arterial wall thickening and RELMa expression in the lung. CC10 IL-25 mice but not CC10 IL-25 NKT-/- mice spontaneously developed pulmonary arterial wall thickening and RELMa expression in the lung at 6 months of age. These results shows that prolonged expression of IL-25 in the lung induces pulmonary arterial wall thickening by NKT cell-dependent mechanisms.
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