Mediators resulting from the action of the cyclooxygenases on arachidonic acid are known as “prostaglandins” (PG) or “thromboxane” (Tx). The oxidative metabolism of cyclooxygenases results in formation of cyclic endoperoxides PGG2 and PGH2. The subsequent action of prostaglandin isomerases produces either PGD2 or PGE2, reductive cleavage produces PGF2α, while one of two terminal synthetases on the operoxide produces PGI2 and TxA2. Prostaglandins and thromboxane mediate their effects through the activation of specific receptors and cross activation of receptors by different agonists. These mediators are significantly relevant in the pathogenesis of asthma. In asthmatic patients, PGD2 and TxA2 are involved in causing acute bronchoconstriction after stimuli. PGE2 also attenuates allergen-induced airway responses and eosinophilic inflammation. Studies suggest that endogenous production of PGE2 has an important influence on the magnitude of asthmatic responses to stimuli such as exercise or inhaled allergens.