Abstract
Prostanoids, consisting of the prostaglandins (PGs) and the thromboxanes (TXs), are a group of lipid mediators formed in response to various stimuli. They include PGD2, PGE2, PGF2α, PGI2, and TXA2. Given that aspirin-like nonsteroidal anti-inflammatory drugs exert their actions by suppressing prostanoid production, prostanoids have been implicated in processes inhibited by these drugs, including inflammation, fever, and pain. However, how prostanoids exert such a variety of actions had remained unclear. Prostanoids are released outside of the cells immediately after synthesis, and exert their actions by binding to receptors on the surface of target cells. We have identified a family of eight types or subtypes of G protein-coupled receptors that mediate prostanoid actions. They are the PGD receptor (DP), four subtypes of the PGE receptor (EP1, EP2, EP3, and EP4), the PGF receptor (FP), PGI receptor (IP), and TXA receptor (TP). Recently mice deficient in each of these prostanoid receptors were generated and subjected to various experimental models of disease. These studies have not only elucidated the molecular and cellular mechanisms of known prostanoid actions but also revealed previously unknown actions. In this article, we review several recent findings of the roles of prostanoid receptor signalling in inflammation, allergy, and immunity.
