Possible role of prostaglandins in allergic inflammation

Abstract

Summary Prostaglandins (PGs) and thromboxanes (TXs) are autacoids that exhibit a wide variety of actions in various cells and tissues. There is persuasive evidence that some PGs contribute to causing signs and symptoms of inflammation. In this study, we investigated the role of PGs and TXs in allergic airway inflammation by using a mouse model. When indomethacin was orally administered to allergic mice, the production of T‐helper type 2 cytokines, IgE antibody, and airway eosinophils and airway responsiveness to acetylcholine were accelerated. We next focused on the role of each PG by using mice lacking specific PG receptor genes. We examined the effects of depletion of PGD2 receptor (DP), PGE2 receptor (EP1, EP3, and EP4), PGI2 receptor (IP), and TxA2 receptor (TP) genes on the development of allergic inflammation in mice. As a result, allergic inflammation in the airway was accelerated in EP3 and IP gene knockout mice whereas inflammation was clearly suppressed in DP and TP gene‐deficient mice. These data suggest that PGE2 and PGI2 might have a suppressive role whereas PGD2 and TxA2 have pathological roles in the development of allergic airway inflammation.