Aspirin-induced asthma: Advances in pathogenesis and management Andrew Szczeklik, MD a, Donald D. Stevenson, MD b  Journal of Allergy and Clinical Immunology  Volume 104, Issue 1, Pages 5-13 (July 1999) DOI: 10.1016/S0091-6749(99)70106-5 Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 1 This illustration could represent either a mast cell or eosinophil, the 2 most prominent cells detected in the respiratory mucosa of patients with AIA. Other inflammatory cells could also participate, although PMNs and macrophages predominantly synthesize LTB 4 . During inflammatory respiratory disease, Cys-LTs, histamine, and eosinophilic cationic protein (ECP) are formed and released, effecting eosinophil recruitment, vascular permeability, mucus secretion, and bronchial hyperreactivity. When ASA is added, the respiratory reaction begins, COX-1 and COX-2 are both disabled, PGE 2 synthesis ceases and its modulating effects on mast cells and 5-LO are removed, and mediators are released or synthesized. If LTC 4 synthase is increased, augmented synthesis of Cys-LTs also occurs. During ASA desensitization, COX-1 and COX-2 continue to be disabled, with concomitant blocking of prostanoid formation. Histamine secretion ceases, but Cys-LTs continue to be synthesized at a rate found at baseline. However, Cys-LT bronchial receptors are downregulated. 5-LO and FLAP enzymes are not different from those of normal subjects and are not directly affected by ASA/NSAIDs. Journal of Allergy and Clinical Immunology 1999 104, 5-13DOI: (10.1016/S0091-6749(99)70106-5) Copyright © 1999 Mosby, Inc. Terms and Conditions