Prostaglandin E2 in NSAID-exacerbated respiratory disease protection against cysteinyl leukotrienes and group 2 innate lymphoid cellsRusznak, Mark; Peebles, R. Stokes Jr.Current Opinion in Allergy and Clinical Immunology: February 2019 - Volume 19 - Issue 1 - p 38–45 doi: 10.1097/ACI.0000000000000498 MECHANISMS OF ALLERGY AND ADULT ASTHMA: Edited by J. Andrew Grant and Enrico Heffler Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The purpose of this review is to describe the recent advances that have been made in understanding the protective role of prostaglandin E2 (PGE2) in aspirin-exacerbated respiratory disease (AERD), known in Europe as NSAID-exacerbated respiratory disease (N-ERD). Recent findings Decreased PGE2 signaling through the EP2 receptor in patients with AERD leads to an increase in leukotriene synthesis and signaling. Leukotriene signaling not only directly activates group 2 innate lymphoid cells and mast cells, but it also increases production of IL-33 and thymic stromal lymphopoietin. These cytokines drive Th2 inflammation in a suspected feed-forward mechanism in patients with AERD. Summary Recent discoveries concerning the role of PGE2 in leukotriene synthesis and signaling in AERD, as well as downstream effects on group 2 innate lymphoid cells and mast cells, allow for a more comprehensive understanding of the pathogenesis of this disease. These discoveries also identify new paths of potential investigation and possible therapeutic targets for AERD. Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA Correspondence to Stokes Peebles, MD, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, T-1218 MCN, VUMC, 1161 21st Ave South, Nashville, TN 37232-2650, USA. Tel.: +615 343 3412;. fax: +615 343 7448; e-mail: email@example.com Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.