Role of Aquaporin-9 in inflammatory skin disease
Project/Area Number |
24591648
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Kyoto University |
Principal Investigator |
CHIKUMA Mariko 京都大学, 医学(系)研究科(研究院), 准教授 (40531736)
|
Co-Investigator(Kenkyū-buntansha) |
MIYACHI Yoshiki 京都大学医学研究科, 皮膚科学講座, 教授 (30127146)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | アクアポリン / 接触皮膚炎 / 細胞遊走 / 好中球 / Aquaporin |
Outline of Final Research Achievements |
Aquaporin-9 (AQP9) is expressed in several immune cells, including neutrophils. Here we show the involvement of AQP9 in hapten-induced contact hypersensitivity (CHS) using AQP9 knockout (AQP9-/-)mice. First, the CHS response to hapten was impaired in AQP9-/- mice compared with wild-type (WT) mice. Second, administration of WT neutrophils into AQP9-/- mice during sensitization rescued the impaired CHS response. Neutrophil recruitment to dLNs upon hapten application was attenuated by AQP9 deficiency. AQP9-/- neutrophils showed a reduced CCR7 ligand-induced migration efficacy, which was attributed to the attenuated recruitment of neutrophils to dLNs. These findings suggest that AQP9 is required for the development of sensitization during cutaneous acquired immune responses via regulating neutrophil function.
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Report
(4 results)
Research Products
(2 results)