| Project/Area Number |
26462723
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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 |
Plastic surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
TAKEDA ATSUSHI 東北大学, 医学系研究科, 非常勤講師 (30333800)
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| Co-Investigator(Kenkyū-buntansha) |
館 正弘 東北大学, 医学系研究科, 教授 (50312004)
川上 和義 東北大学, 医学系研究科, 教授 (10253973)
菅野 恵美 東北大学, 医学系研究科, 講師 (10431595)
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| Research Collaborator |
TAKAGI Naoyuki 東北大学, 医学系研究科, 助教
TANNO Hiromasa 東北大学, 医学系研究科, 助教
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 創傷治癒 / IL-17 / サイトカイン / 創傷治癒学 |
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| Outline of Final Research Achievements |
Interleukin-17 (IL-17) is a proinflammatory cytokine. The role of this cytokine in the wound healing process is not fully clarified. In this study, IL-17A knockout mice showed promoted wound healing and decreased neutrophil accumulation compared with wild-type mice, and the administration of recombinant IL-17A led to delayed wound closure, accelerated neutrophilic accumulation and improved wound repair with treatment of a neutrophil elastase inhibitor. Neutrophils, macrophages and gamma-delta T cels showed IL-17A expression after wounding in wild-type mice.
These results indicated that IL-17A hampared the wound healing process and neutrophilic inflammation caused by IL-17 led to impaired wound healing in skin.
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