Regulation of Allergic Responses by Prostaglandins: A Review

SRSA-mediated bronchospasm by pharmacologic modification of lung anaphylaxis in vivo

“…The use of methysergide (a serotonin antagonist), or bilateral vagotomy, had no inhibitory effect on antigen-induced bronchospasm (data not shown), suggesting very little role of serotonin or reflex vagal bronchoconstriction in anaphylactic bronchospasm in the anesthetized guinea pig. Since inhibition of cyclooxygenase with indomethacin increased the histamine-antagonized, antigen-induced bronchospasm, then either: (1) arachidonic acid metabolism via cyclooxygenase results in the production of bronchodilating prostaglandins which are no longer made in the presence of indomethacin; (2) the available arachidonic acid is metabolized by an alternate pathway to a bronchoconstrictory substance; or (3) both [38]. Since arachidonic acid (AA) induced bronchospasm in the unsensitized guinea pig can be blocked by indomethacin or thromboxane antagonists [39], bronchodilating prostaglandins are probably not the major products of AA metabolism by cyclooxygenase in the guinea pig.…”

Successful Treatment of Recalcitrant Primary Follicular Mucinosis with Indomethacin and Low-dose Intralesional Interferon Alpha

“…The exact mechanism of the effect of indomethacin and IFN α on FM is not well established. Indomethacin is an inhibitor of cyclooxygenase activity that reduces the synthesis of eosinophil chemotactic factor and lymphokine, resulting in the inhibition of the chemataxis of eosinophils and the inhibited activation of lymphocytes and macrophages 10,11 . IFN α has imunomodulatory effects, which include enhancement of suppressor T cells and inhibition of the helper T cell function, and a stimulating effect on the phagocytic and metabolic activities of macrophages 12,13 .…”

Prostaglandins, hydroxy fatty acids, leukotrienes and inflammation of the skin

“…However, the picture is complicated by the demonstrated effects of certain prostaglandins on infiammatory cells. While none of the prostaglandins has been shown to be significantly chemotactic in man, there is evidence that prostaglandins E,, E2 and 12 may inhibit some functions of mast cells, lymphocytes and polymorphonuclear leucocytes by virtue of their ability to stimulate cellular adenyl cyclase, thereby increasing intracellular levels of cyclic AMP (Weissmann, Smolen & Korchak, 1980;Morley et al, 1980;Goldyne, 1977). This has led to the belief that these prostaglandins may have anti-infiammatory effects, and that some inflammatory reactions may be potentiated by treatment with cyclo-oxygenase inhibitors such as indomethacin and aspirin.…”