Prostaglandin E2 in NSAID-exacerbated respiratory disease: protection against cysteinyl leukotrienes and group 2 innate lymphoid cells

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.

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