A truncated mutation of MucA in Pseudomonas aeruginosa from a bronchiectasis patient affects T3SS expression and inflammasome activation.

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic airway infection in bronchiectasis patients and is closely associated with poor prognosis. Strains isolated from chronically infected patients typically have a mucoid phenotype due to the overproduction of alginate. In this study, we isolate a P. aeruginosa strain from the sputum of a patient with bronchiectasis and find that a truncated mutation occurred in mucA, which is named mucA117. mucA117 causes the strain to transform into a mucoid phenotype, downregulates the expression of T3SS and inflammasome ligands such as fliC and allows it to avoid inflammasome activation. The truncated mutation of the MucA protein may help P. aeruginosa escape clearance by the immune system, enabling long-term colonization.