Distinct contributions of interleukin-1α (IL-1α) and IL-1β to innate immune recognition of Pseudomonas aeruginosa in the lung.

ABSTRACT: The bacterial pathogen Pseudomonas aeruginosa causes acute infections associated with significant morbidity and mortality. P. aeruginosa elicits strong innate immune responses in immunocompetent hosts, and the resulting recruitment of neutrophils to the site of infection is necessary for bacterial clearance. P. aeruginosa lipopolysaccharide and flagellin are recognized by extracellular Toll-like receptors, but the most rapid responses to infection occur when cytosolic receptors sense flagellin or type 3 secretion system (T3SS) structural proteins. The subsequent activation of the NLRC4 inflammasome and caspase-1 generates an interleukin-1β (IL-1β) signal that is required for the rapid neutrophilic response. A T3SS effector, exotoxin U (ExoU), can inhibit activation of the NLRC4 inflammasom

SUBMITTER: Al Moussawi K 

PROVIDER: S-EPMC4187872 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature