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Metabolic and transcriptional activities underlie stationary-phase Pseudomonas aeruginosa sensitivity to Levofloxacin.

ABSTRACT:

Importance

The bacterial pathogen Pseudomonas aeruginosa is responsible for a variety of chronic human infections. Even in the absence of identifiable resistance mutations, this pathogen can tolerate lethal antibiotic doses through phenotypic strategies like biofilm formation and metabolic quiescence. In this study, we determined that P. aeruginosa maintains greater metabolic activity in the stationary phase compared to the model organism, Escherichia coli, which has traditionally been used to study fluoroquinolone antibiotic tolerance. We demonstrate that hallmarks of E. coli fluoroquinolone tolerance are not conserved in P. aeruginosa, including the timing of cell death and necessity of the SOS DNA damage response for survival. The heightened sensitivity of stationary-phase P. aeruginosa to fluoroquinolones is attributed to maintained transcriptional and reductase activity. Our data suggest that perturbations that suppress transcription and respiration in P. aeruginosa may actually protect the pathogen against this important class of antibiotics.

SUBMITTER: Hare PJ

PROVIDER: S-EPMC10896071 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Metabolic and transcriptional activities underlie stationary-phase <i>Pseudomonas aeruginosa</i> sensitivity to Levofloxacin.

Hare Patricia J PJ Gonzalez Juliet R JR Quelle Ryan M RM Wu Yi I YI Mok Wendy W K WWK

Microbiology spectrum 20231211 1

<h4>Importance</h4>The bacterial pathogen <i>Pseudomonas aeruginosa</i> is responsible for a variety of chronic human infections. Even in the absence of identifiable resistance mutations, this pathogen can tolerate lethal antibiotic doses through phenotypic strategies like biofilm formation and metabolic quiescence. In this study, we determined that <i>P. aeruginosa</i> maintains greater metabolic activity in the stationary phase compared to the model organism, <i>Escherichia coli</i>, which has ...[more]

PMID: 38078717

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