Prostaglandin E(2)-EP3 signaling suppress skin inflammation in mouse contact hypersensitivity.
| Project/Area Number |
20790798
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Kyoto University |
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Principal Investigator |
HONDA Tetsuya Kyoto University, 医学研究科, 助教 (40452338)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| 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)
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| 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 |
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| 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.
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Report
(3 results)
Research Products
(3 results)
