Identification of Anti-virulence Compounds That Disrupt Quorum-Sensing Regulated Acute and Persistent Pathogenicity (original) (raw)
Figure 3
The most potent inhibitors reduce 2-AA production and the formation of antibiotic tolerant persisters.
a. 2-AA levels in presence of 10 µM inhibitor. Error bars show mean +/− SD of at least 2 replicates. b. Observed fold change in persister cell concentrations of PA14 cultures with 10 µM inhibitor or with 0.75 mM 2-AA. Untreated PA14 cells and mvfR- cells were the positive and negative controls, respectively. Error bars show mean +/− SEM of at least 3 replicates. Differences between PA14 and the samples M34, M50, M62, M59, M51, M64 or mvfR- (p<0.01) as well as between PA14 and the samples PA14 + 2-AA or M29 (p<0.01) are statistically significant (one way ANOVA, Dunnett's test). c. Observed fold change in persister cell concentrations of PA14 plus 5 µM M64 in the presence of clinical antibiotics used to treat P. aeruginosa infections: amikacin (blue), levofloxacin (purple), ciprofloxacin (orange) and meropenem (red). All values were normalized to control cultures in 0.01% DMSO. Error bars show mean +/− SEM of at least 3 replicates. Differences between control and the samples amikacin, levofloxacin, ciprofloxacin or meropenem are statistically significant (p<0.01, one way ANOVA, Dunnett's test).