Antimicrobial Potential of Carvacrol against Uropathogenic Escherichia coli via Membrane Disruption, Depolarization, and Reactive Oxygen Species Generation

Abstract

Bacterial resistance to antibiotics poses a serious threat to cure diseases associated with microbial infection. Among the resistant bacteria, extended-spectrum β-lactamase (ESBL)-producing bacteria are the most concerned one as they encode the enzyme β-lactamase that confers resistance to most β-lactam antibiotics. The present study was carried out to determine the antimicrobial potential and the principle mechanism of action of carvacrol against ESBL <i>Escherichia coli</i> isolated from ascitic fluid of a patient having a urinary tract infection. Carvacrol exhibited a minimum inhibitory concentration (MIC) of 450 μg/ml at which it reduced <i>E. coli</i> cell counts significantly in a time-dependent manner. Carvacrol completely diminished the growth of <i>E. coli</i> after 2 h of incubation at its MIC. Fluorescent imaging displayed the elevated reactive oxygen species level and bacterial membrane depolarization leading to <i>E. coli</i> cell death in presence of carvacrol at its MIC. Furthermore, carvacrol displayed a severe detrimental effect on bacterial membrane disruption and cellular material release. In addition, a significant effect of carvacrol at sub-inhibitory concentration was observed on motility of <i>E. coli</i> cells and invasion of human colon HCT-116 cells in an <i>ex vivo</i> model. Based on the results, we conclude a potential antimicrobial role of carvacrol against ESBL <i>E. coli</i>.