Pseudomonas aeruginosa sabotages the generation of host proresolving lipid mediators.

ABSTRACT: Recurrent Pseudomonas aeruginosa infections coupled with robust, damaging neutrophilic inflammation characterize the chronic lung disease cystic fibrosis (CF). The proresolving lipid mediator, 15-epi lipoxin A₄ (15-epi LXA₄), plays a critical role in limiting neutrophil activation and tissue inflammation, thus promoting the return to tissue homeostasis. Here, we show that a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhibitory factor (Cif), can disrupt 15-epi LXA₄ transcellular biosynthesis and function. In the airway, 15-epi LXA₄ production is stimulated by the epithelial-derived eicosanoid 14,15-epoxyeicosatrienoic acid (14,15-EET). Cif sabotages the production of 15-epi LXA₄ by rapi

SUBMITTER: Flitter BA 

PROVIDER: S-EPMC5224368 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature