Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes. Mast cells and eosinophils have roles in mediating many of the observed effects. Increased levels of both interleukin-4 (IL-4) and interferon (IFN)-γ are present in the tissue of patients with AERD. Previous studies showed that IL-4 is primarily responsible for the upregulation of LTC4S by mast cells. Our studies show that IFN-γ, but not IL-4, drives this process in eosinophils. This article examines the overall role that eosinophils and mast cells contribute to the pathophysiology of AERD.
Keywords: Arachidonic acid; Aspirin-exacerbated respiratory disease; Cyclooxygenase; Eosinophil; Leukotriene; Mast cell; Prostaglandin.
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