Suppression of aspirin-mediated eosinophil activation by prostaglandin E2: Relevance to aspirin/NSAID hypersensitivity.

CONCLUSION: Eosinophils can be directly activated by NSAIDs via cyclooxygenase independent pathways to produce CysLTs and LTB4. This effect can be inhibited by PGE2 acting through the EP2 receptor. The recognized loss of EP2 receptor expression combined with low PGE2 levels, explain in part the sensitivity to NSAIDs.
PMID: 31513909 [PubMed - as supplied by publisher]

Source: Annals of Allergy, Asthma and Immunology - September 8, 2019 Category: Allergy & Immunology Authors: Pal K, Ramsden M, Shim YM, Borish L, Payne SC, Steinke JW Tags: Ann Allergy Asthma Immunol Source Type: research