ABSTRACT
Allergen inhalation by allergic asthmatics can result in the occurrence of an immediate, acute bronchoconstriction that peaks 10-20 min and resolves 1-2 h after allergen exposure. The acute response is thought to be the result of the release of bronchoactive and vasoactive mediators from resident airway cells resulting in a rapid smooth muscle constriction, mucus secretion and edema formation. Numerous cell types have been implicated in the pathogenesis of the late-phase response, including eosinophils, platelets, and neutrophils. Each of these cells is well-equipped and quite capable of altering airway function by the release of biologically active, preformed granule-associated mediators as well as newly synthesized membrane-derived lipid mediators, including platelet activating factor (PAF), leukotrienes and prostaglandins. Neutrophils generate lipid mediators such as prostaglandins and PAF in response to many different stimuli including major basic protein.
