A mouse model of AERD: Prostaglandin E2 (PGE2) deficiency results in AERD-like phenotype

Prostaglandin E2 (PGE2) deficiency results in AERD-like phenotype.

AERD/Samter’s Triad is characterized by mast cell activation with overproduction of cysteinyl leukotrienes following inhibition of COX-1 by medications like aspirin or NSAIDs. The cause of the mast cell activation that occurs following COX-1 inhibition is unknown.
Recent work in the Boyce Lab by Liu et al revealed that in a mouse model of dust mite-induced asthma, impairment in PGE2 production following challenge with aspirin in an inflamed lung resulted in an AERD-like phenotype that was dependent upon platelets and thromboxane receptors. Aspirin challenge in these mice resulted in overproduction of cysteinyl leukotrienes that led to mast cell activation, thereby showing that the scientists had for the first time created a mouse model of AERD. This is a leap forward in the field, as some of the authors’ findings suggest potential new targets for therapy, and the future applications of a mouse model as a research tool are endless.