Analysis of role of aryl hydrocarbon receptor for pathophysiology of atopic dermatitis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461688
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• 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)
• Project Period (FY): 2013-04-01 – 2016-03-31
• 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.

Free Research Field

皮膚科学