Effects of the released mediators of anaphylaxis on the target organs.
The antigen-antibody union initiates the release of mediators; the reactions and interactions of these mediators in the lung appear to include negative feedback mechanisms. During anaphylactic bronchoconstriction catecholamines are released from the adrenal medulla. These act as physiological antagonists and tend to reverse the bronchoconstriction. In guinea-pig and human lung fragments, catecholamines and PGs increase cyclic AMP levels and inhibit the release of histamine, SRS-A and ECF-A following antigen challenge. EFC-A is chemotactic to eosinophils which contain arylsulphatase which destroys SRS-A. Aanphylactic bronchoconstriction seems to be a defense mechanism to limit further inhalation of antigen by the animal. It then seems that a series of negative feedback mechanisms may be triggered to terminate and reverse the bronchoconstriction and prevent further release of mediators.
D000707:Anaphylaxis; D000818:Animals; D001920:Bradykinin / Q000502:physiology; D001980:Bronchi / Q000276:immunology; D002395:Catecholamines / Q000502:physiology; D002417:Cattle; D006168:Guinea Pigs; D006636:Histamine Release; D006801:Humans; D007610:Kallikreins / Q000502:physiology; D008168:Lung / Q000276:immunology; D011458:Prostaglandins E / Q000502:physiology; D011460:Prostaglandins F / Q000502:physiology; D013189:SRS-A / Q000502:physiology; D013928:Thromboxane A2 / Q000502:physiology
D002395:Catecholamines; D011458:Prostaglandins E; D011460:Prostaglandins F; D013189:SRS-A; D013928:Thromboxane A2; D007610:Kallikreins; D001920:Bradykinin