Prostaglandin E(2)-EP3 signaling suppress skin inflammation in mouse contact hypersensitivity.

Research Project

Project/Area Number	20790798
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Dermatology
Research Institution	Kyoto University
Principal Investigator	HONDA Tetsuya Kyoto University, 医学研究科, 助教 (40452338)
Project Period (FY)	2008 – 2009
Project Status	Completed (Fiscal Year 2009)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords	プロスタグランジンE2 EP3受容体 / 接触皮膚炎 / アレルギー・喘息 / 免疫 / プロスタグランジン
Research Abstract	Prostaglandin E2 is a lipid mediator, and EP3 is one of the receptor of PGE2. Administration of a EP3 selective agonist significantly suppressed mouse contact hypersensitivity response. EP3 signaling inhibited chemokine production from keratinocytes and suppressed inflammatory cell infiltration in contact hypersensitivity.

Report

(3 results)