Pseudomonas aeruginosa utilises the host-derived polyamine spermidine to facilitate antimicrobial tolerance.

ABSTRACT: Pseudomonas aeruginosa undergoes diversification during infection of the cystic fibrosis (CF) lung. Understanding these changes requires model systems that capture the complexity of the CF lung environment. We previously identified loss-of-function mutations in the two-component regulatory system sensor kinase gene pmrB, in P. aeruginosa from CF and from experimental infection of mice. Here, we demonstrate that whilst such mutations lower in vitro MICs for multiple antimicrobial classes, this is not reflected in increased antibiotic susceptibility in vivo. Loss of PmrB impairs aminoarabinose modification of lipopolysaccharide, increasing the negative charge of the outer membrane and promoting uptake of cationic antimicrobials. However, in vivo, this can be offset by increased membrane bind

SUBMITTER: Hasan CM 

PROVIDER: S-EPMC9746822 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature