| Project/Area Number |
15K09254
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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 |
Kidney internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
安田 日出夫 浜松医科大学, 医学部附属病院, 講師 (60432209)
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| Co-Investigator(Renkei-kenkyūsha) |
SUGIMOTO Ken 浜松医科大学, 医学部, 准教授 (20529507)
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| Research Collaborator |
TSUJI Naoko
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 急性腎障害 / 敗血症 / TLR9 / IL-17 |
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| Outline of Final Research Achievements |
It has not been elucidated that the downstream of Toll-like receptor 9 (TLR9) pathway in septic acute kidney injury (AKI). We hypothesized that Interleukin (IL)-17A plays a central role in it. Septic AKI was induced by cecal ligation and puncture (CLP). IL-17A knockout (KO) mice exhibited decreased serum creatinine levels and improved tubular damage score in cortex at 18 hours after CLP. Systemic inflammatory cytokines and splenic apoptosis were decreased at 18 hours after CLP in IL-17AKO mice compared with Wild type (WT) mice. Mortalities were less in IL-17AKO mice compared with WT mice after CLP. IL-17A levels of plasma were significantly higher in WT mice than Tlr9KO mice at 18 hours after CLP. Although IL-17A production of splenic γδ T cells in WT mice was increased at 3 hours after CLP, its in Tlr9KO mice was suppressed. These findings suggest that TLR9 mediates IL-17A production in septic AKI.
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