Analysis of role of aryl hydrocarbon receptor for pathophysiology of atopic dermatitis
Project/Area Number |
25461688
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
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Research Institution | Shinshu University |
Principal Investigator |
OGAWA Eisaku 信州大学, 学術研究院医学系, 助教 (20451586)
|
Co-Investigator(Kenkyū-buntansha) |
KINIWA Yukiko 信州大学, 学術研究院医学系(医学部付属病院), 講師 (20436893)
OKUYAMA Ryuhei 信州大学, 学術研究院医学系, 教授 (80292332)
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Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | AhR / アトピー性皮膚炎 |
Outline of Final Research Achievements |
To elucidate the mechanism how to induce inflammation in atopic dermatitis, I focused aryl hydrocarbon receptor (AhR) signaling pathway. I seeked candidates which are induced under AhR activation by using previous transgenic mouse model and AhR-overexpressed cultured keratinocyte. So I identified increasing expression of interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP), which were both related in atopic dermatitis recently. I observed increase expression of IL-33 and TSLP in culutured keratinocyte after the addition of AhR activator. These data suggest that AhR activation induced expression of IL-33 and TSLP in keratinocyte. Taken together, AhR activation might induce early inflammation like atopic dermatitis.
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Report
(4 results)
Research Products
(4 results)