Comparative <i>in vitro</i> activity of various antibiotic against planktonic and biofilm and the gene expression profile in <i>Pseudomonas aeruginosa</i>

Abstract

<abstract> <p><italic>P. aeruginosa</italic> is an opportunistic pathogen that is commonly found in nosocomial infections. The purpose of this study was to investigate the effects of seven antibiotics on <italic>P. aeruginosa</italic> planktonic growth, biofilm formation, and the expression of virulence factors. These antibiotics included Ciprofloxacin (CP), Amikacin (AMK), Vancomycin (VAN), Tetracycline (TET), Gentamicin (GEN), Erythromycin (Ery), and Clindamycin (CLI). Antibiotic susceptibility testing, Minimum Bactericidal Concentration (MBC), Minimum Inhibitory Concentration (MIC), growth curve, time-kill curve, biofilm inhibition and reduction assay, and RT-qPCR were used to assess the effects of these antibiotics on <italic>P. aeruginosa</italic> planktonic and biofilm. The clear zones of inhibition against <italic>P. aeruginosa</italic> for the CP, AMK, VAN, TET, GEN, Ery, and CLI were 26 mm, 20 mm, 21 mm, 22 mm, 20 mm, 25 mm and 23 mm, respectively. The MIC values for CP, AMK, VAN, TET, GEN, Ery and CLI against <italic>P. aeruginosa</italic> ranged from 0.25 to 1 µg/mL while the MBC values ranged from 1 and 0.5 to 2 µg/mL respectively. The growth, total viable counts (TVCs), bacterial adhesion and biofilm formation of <italic>P. aeruginosa</italic> were reduced after exposure to all the tested antibiotics in a dose-dependent manner. The RT-qPCR analysis showed that all the tested antibiotics share a similar overall pattern of gene expression, with a trend toward reduced expression of the virulence genes of interest (<italic>lasR, lasI, fleN, fleQ and fleR, oprB</italic> and <italic>oprC</italic>) in <italic>P. aeruginosa</italic>. The results indicate that all of the tested antibiotics possess antimicrobial and anti-biofilm activities, and that they may be multiple inhibitors and moderators of <italic>P. aeruginosa</italic> virulence via a variety of molecular targets. This deduction requires to be investigated <italic>in vivo</italic>.</p> </abstract>