| Project/Area Number |
23390217
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Keio University |
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Principal Investigator |
SANO MOTOAKI 慶應義塾大学, 医学部, 准教授 (30265798)
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| Co-Investigator(Renkei-kenkyūsha) |
YAN Xiaoxiang 慶應義塾大学, 医学部, 大学院生 (90594979)
ANZAI Atsushi 慶應義塾大学, 医学部, 助教 (50528164)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2013: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2012: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2011: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Keywords | 心筋梗塞 / 心不全 / 免疫 / 肺水腫 / NK細胞 / 好中球 / IL-10 / 線維化 / 樹状細胞 / リンパ球 / マクロファージ |
|---|
| Research Abstract |
Left ventricular (LV) remodeling leads to chronic heart failure and is a main determinant of morbidity and mortality after myocardial infarction (MI). Mice with DC ablation showed deteriorated LV function and remodeling concomitant with enhanced expression of IL-1beta, IL-18, and TNF-alpha, prolonged extracellular matrix degradation, marked infiltration of proinflammatory monocytes. A deficiency of gamma-delta T cells improved survival, limiting infarct expansion and fibrosis in noninfarcted myocardium and alleviating LV dilatation and systolic dysfunction after MI. IL-17A-producing gamma-delta T cells promotes sustained infiltration of neutrophils and macrophages, , aggravating cardiomyocyte death, and enhancing fibroblast proliferation. Depletion of NK cells from mice exhibited severe respiratory. Adoptive transfer of NK cells from wild-type mice, but not from IL-10 knockout mice, into the NK cell-depleted mice rescued the respiratory phenotype.
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