Abstract
The emergence of carbapenem-resistant Enterobacterales (CRE) seriously limits treatment options for bacterial infections. Combined drugs are an effective strategy to treat these resistant strains. This study aimed to evaluate the synergistic effect of equol and meropenem against carbapenem-resistant Escherichia coli. First, this study investigated the antibacterial activity of carbapenems on clinically isolated E. coli strains by analyzing the minimum inhibitory concentrations (MICs). The E. coli strains were all resistant to carbapenem antibiotics. Therefore, we confirmed the cause of carbapenem resistance by detecting blaKPC and blaOXA-48 among the carbapenemase genes using polymerase chain reaction (PCR) analysis. Checkerboard and time-kill analyses confirmed that equol restored the susceptibility of carbapenem-resistant E. coli to meropenem. Also, the transcription levels of specific carbapenemase genes in E. coli were significantly suppressed by equol. The study also evaluated the anti-virulence effects of equol on bacterial biofilm and motility through phenotypic and genotypic analyses. In conclusion, our results revealed that equol had a synergistic effect with meropenem on carbapenem-resistant E. coli. Therefore, this study suggests that equol is a promising antibiotic adjuvant that prevents the expression of carbapenemases and virulence factors in carbapenem-resistant E. coli.
Highlights
Carbapenems are antibiotics used to treat multidrug-resistant (MDR) bacterial infections as a last resort
This study investigated the mechanisms related to carbapenem-resistant E. coli and the synergistic effect of equol combined with meropenem
E. coli strains were identically inhibited in terms of cell growth by 90% at
Summary
Carbapenems are antibiotics used to treat multidrug-resistant (MDR) bacterial infections as a last resort. Carbapenem resistance is mediated by several factors such as porin loss, overexpressed efflux pumps, and carbapenemase production [2]. Among these factors, previous studies have reported that the production of carbapenemases is the main mechanism of carbapenem resistance [3,4]. Certain pathogenic strains can cause intestinal and extra-intestinal diseases such as urinary tract infections, meningitis, sepsis, and hemorrhagic colitis by damaging host cells through virulence factors [7]. The virulence factors of E. coli include flagella-mediated motility and curli fibers, which promote biofilm development and pathogenicity [8,9]. A community of sessile cells encased in extracellular polysaccharides self-produced by
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