Journal of Asthma and Allergy (Oct 2020)
The Role of Mast Cells in Aspirin-Exacerbated Respiratory Disease (AERD) Pathogenesis: Implications for Future Therapeutics
Abstract
Merin E Kuruvilla,1 Kristine Vanijcharoenkarn,1 Joshua M Levy2 1Division of Pulmonary, Allergy, Critical Care & Sleep Medicine, Emory University School of Medicine, Atlanta, GA, USA; 2Department of Otolaryngology – Head & Neck Surgery, Emory University School of Medicine, Atlanta, GA, USACorrespondence: Joshua M LevyEmory University School of Medicine, 550 Peachtree St NE, 11th Floor, Atlanta, GA 30308, USAEmail [email protected]: Mast cells (MC) have recently been demonstrated to play an integral role in the pathogenesis of aspirin-exacerbated respiratory disease (AERD). When activated, MCs release pre-formed granules of many pro-inflammatory mediators, including histamine, serotonin, and various chemokines and cytokines including tumor necrosis factor (TNF)-α, interferon ɣ (IFN ɣ), macrophage inhibitory factor, transforming growth factor, interleukin (IL) 1, 3– 6, 9, 10, 13 and 16. These mediators promote inflammation in AERD by recruiting or activating a network of cells involved in acute and chronic inflammatory pathways, such as endothelial, epithelial, stromal, and other immune cells. Several studies have implicated multifactorial pathways for MC activation in AERD beyond classical IgE mediated mechanisms. The elucidation of these complex networks therefore represents important targets for innovative patient therapeutics. This review summarizes classic and alternative pathways of MC activation in AERD with a special focus in relation to new and emerging treatment strategies.Keywords: mast cells, aspirin-exacerbated respiratory disease, asthma, drug sensitivity, humanized monoclonal antibody
