2012 Fiscal Year Final Research Report
Analysis of role of aryl hydrocarbon receptor for pathophysiology of atopic dermatitis
| Project/Area Number |
23791262
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Shinshu University |
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Principal Investigator |
OGAWA Eisaku 信州大学, 医学部, 助教 (20451586)
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| Project Period (FY) |
2011 – 2012
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| Keywords | Ahr / アトピー性皮膚炎 |
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| Research Abstract |
To elucidate the mechanism how to induce inflammation in atopic dermatitis, I focused aryl hydrocarbon receptor (AhR) signaling pathway. In the recent study, Tauchi M et al. showed that constitutive expression of aryl hydrocarbon receptor in keratinocytes causes atopic dermatitis-like skin lesions in transgenic mouse.Their discovery is very intriguing because secretion production by keratinocyte cause skin inflammation. And their skin inflammation is like atopic dermatitis. 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 some proinflammatory cytokines, which may be related in atopic-like dermatitis. I observed increase expression of them in culutured keratinocyte after the addition of AhR activator. These data suggest that AhR activation induced expression of some proinflammatory cytokines in keratinocyte.In atopic dermatitis, dendritic cell has a significant role in establishment of inflamation. I speculate that AhR activation in keratinocyte induce dendritic cell activity.
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