E-prostanoid-3 receptors mediate the proinflammatory actions of prostaglandin E2 in acute cutaneous inflammation.

Journal Article (Journal Article)

PGs are derived from arachidonic acid by PG-endoperoxide synthase (PTGS)-1 and PTGS2. Although enhanced levels of PGs are present during acute and chronic inflammation, a functional role for prostanoids in inflammation has not been clearly defined. Using a series of genetically engineered mice, we find that PTGS1 has the capacity to induce acute inflammation, but PTGS2 has negligible effects on the initiation of this response. Furthermore, we show that the contribution of PTGS1 is mediated by PGE(2) acting through the E-prostanoid (EP)3 receptor. Moreover, in the absence of EP3 receptors, inflammation is markedly attenuated, and the addition of nonsteroidal anti-inflammatory agents does not further impair the response. These studies demonstrate that PGE(2) promotes acute inflammation by activating EP3 receptors and suggest that EP3 receptors may be useful targets for anti-inflammatory therapy.

Full Text

Duke Authors

Cited Authors

  • Goulet, JL; Pace, AJ; Key, ML; Byrum, RS; Nguyen, M; Tilley, SL; Morham, SG; Langenbach, R; Stock, JL; McNeish, JD; Smithies, O; Coffman, TM; Koller, BH

Published Date

  • July 15, 2004

Published In

Volume / Issue

  • 173 / 2

Start / End Page

  • 1321 - 1326

PubMed ID

  • 15240726

International Standard Serial Number (ISSN)

  • 0022-1767

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.173.2.1321


  • eng

Conference Location

  • United States