Suppression of allergic inflammation by the prostaglandin E receptor subtype EP3

  • Tomonori Kunikata1 Hana Yamane2, 4, Eri Segi1, 4, Toshiyuki Matsuoka1, 4, Yukihiko Sugimoto2, Satoshi Tanaka2, Hiroyuki Tanaka3, Hiroichi Nagai3, Atsushi Ichikawa2 & Shuh Narumiya  
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Abstract

Prostaglandins, including PGD2 and PGE2, are produced during allergic reactions. Although PGD2 is an important mediator of allergic responses, aspirin-like drugs that inhibit prostaglandin synthesis are generally ineffective in allergic disorders, suggesting that another prostaglandin-mediated pathway prevents the development of allergic reactions. Here we show that such a pathway may be mediated by PGE2 acting at the prostaglandin E receptor EP3. Mice lacking EP3 developed allergic inflammation that was much more pronounced than that in wild-type mice or mice deficient in other prostaglandin E receptor subtypes. Conversely, an EP3-selective agonist suppressed the inflammation. This suppression was effective when the agonist was administered 3 h after antigen challenge and was associated with inhibition of allergy-related gene expression. Thus, the PGE2-EP3 pathway is an important negative modulator of allergic reactions.

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Authors

  •  4 Tomonori Kunikata1 Hana Yamane2, 4, Eri Segi1, 4, Toshiyuki Matsuoka1, 4, Yukihiko Sugimoto2, Satoshi Tanaka2, Hiroyuki Tanaka3, Hiroichi Nagai3, Atsushi Ichikawa2 & Shuh Narumiya

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