Key result
EP3 receptor absence markedly attenuates acute cutaneous inflammation by preventing PGE2 activation.
Why the study?
A functional role for prostanoids in inflammation has not been clearly defined despite enhanced levels of prostaglandins during acute and chronic inflammation.
PGE2 promotes acute inflammation by activating EP3 receptors, suggesting EP3 receptors as potential targets for anti-inflammatory therapy.
EP3 antagonism may attenuate acute inflammation; animal data leaves open human translation and clinical testing.
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.
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Goulet et al. (2004) studied Acute cutaneous inflammation. EP3 receptor absence vs. Presence of EP3 receptors was evaluated on Acute inflammation response. Absence of EP3 receptors markedly attenuated acute cutaneous inflammation, demonstrating that PGE(2) promotes inflammation by activating EP3 receptors.
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