Prostaglandin E2 resistance in granulocytes from patients with aspirin-exacerbated respiratory disease.

ABSTRACT:

Background

Aspirin-exacerbated respiratory disease (AERD) is an inflammatory condition of the respiratory tract and is characterized by overproduction of leukotrienes (LT) and large numbers of circulating granulocyte-platelet complexes. LT production can be suppressed by prostaglandin E(2) (PGE(2)) and the cyclic AMP-dependent protein kinase A (PKA).

Objective

To determine if PGE(2)-dependent control of LT production by granulocytes is dysregulated in AERD.

Methods

Granulocytes from well-characterized patients with and without AERD were activated ex vivo and subjected to a range of functional and biochemical analyses.

Results

Granulocytes from subjects with AERD generated more LTB4 and cysteinyl LTs than did granulocytes from controls with aspirin-tolerant asth

SUBMITTER: Laidlaw TM 

PROVIDER: S-EPMC4040319 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature