Suppression of allergic inflammation by the prostaglandin E receptor subtype EP3

Nat Immunol. 2005 May;6(5):524-31. doi: 10.1038/ni1188. Epub 2005 Apr 3.


Prostaglandins, including PGD(2) and PGE(2), are produced during allergic reactions. Although PGD(2) 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 PGE(2) 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 PGE(2)-EP3 pathway is an important negative modulator of allergic reactions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / immunology
  • Allergens / pharmacology
  • Animals
  • Dinoprostone / agonists
  • Gene Deletion
  • Gene Expression Regulation
  • Hypersensitivity / genetics
  • Hypersensitivity / immunology
  • Hypersensitivity / metabolism*
  • Hypersensitivity / pathology*
  • Inflammation / genetics
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Lung / metabolism
  • Lung / pathology
  • Mice
  • Mice, Knockout
  • Receptors, Prostaglandin E / agonists
  • Receptors, Prostaglandin E / deficiency
  • Receptors, Prostaglandin E / genetics
  • Receptors, Prostaglandin E / metabolism*
  • Receptors, Prostaglandin E, EP3 Subtype


  • Allergens
  • Ptger3 protein, mouse
  • Receptors, Prostaglandin E
  • Receptors, Prostaglandin E, EP3 Subtype
  • Dinoprostone