Th2 profile abrogates cutaneous barrier function. -New insight in the pathogenesis of atopic dermatitis-

Research Project

Project/Area Number	20591323
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Dermatology
Research Institution	Oita University
Principal Investigator	HATANO Yutaka Oita University, 医学部, 講師 (80336263)
Co-Investigator(Kenkyū-buntansha)	KATAGIRI Kazumoto 獨協医科大学, 越谷病院, 教授 (00204420)
Project Period (FY)	2008 – 2010
Project Status	Completed (Fiscal Year 2010)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2010: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000) Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000) Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Keywords	Th2サイトカイン / 皮膚バリア機能 / アトピー性皮膚炎 / コルネオデスモゾーム / デスモグレイン1 / PPARα
Research Abstract	1. Th2 cytokines inhibit the permeability barrier recovery via reduction of formation and secretion of lamellar bodies. 2. Th2 cytokines abrogate integrity of stratum corneum via reduction of density of corneodesmosomes, which results from inhibitory effects of Th2 cytokines on expression of desmoglein 1. 3. Th2 cytokines reduce the expression of PPARα in epidermis, resulting in barrier abnormality in atopic dermatitis. These results suggest that Th2 cytokines are involved in making atopic dermatitis refractory and that activation of PPARα might be one of the new therapeutic targets in atopic dermatiris.