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ABSTRACT: Background
Aspirin-exacerbated respiratory disease (AERD) differs from aspirin-tolerant disease in part because of eosinophilic tissue infiltration and overexpression of arachidonic acid metabolic pathway components that lead to enhanced secretion of cysteinyl leukotrienes and prostaglandin (PG) D2 observed constitutively and paradoxically in response to aspirin and other COX inhibitors. We have previously demonstrated the capacity of IFN-γ to drive cysteinyl leukotriene expression and response.Objective
We investigated eosinophils as a source of PGD2 production in patients with AERD.Methods
Eosinophils were enriched from tissue and peripheral blood obtained from control subjects, patients with aspirin-tolerant disease, and patients with AERD.
SUBMITTER: Feng X
PROVIDER: S-EPMC5056805 | biostudies-literature | 2016 Oct
REPOSITORIES: biostudies-literature