Inhibition effect of kaolinite on the development of antibiotic resistance genes in Escherichia coli induced by sublethal ampicillin and its molecular mechanism

Abstract

Environmental contextAntibiotic resistance by microorganisms in the natural environment poses a threat to ecosystems and public health. We report findings suggesting kaolinite can effectively inhibit the development of antibiotic resistance genes in microorganisms, and present a new understanding of the molecular mechanisms that promote the development of antibiotic resistance. These results are critical to mitigating environmental and public health risks resulting from the abuse of antibiotics. AbstractAntibiotic resistance and antibiotic resistance genes (ARGs) in the natural environment pose a threat to ecosystems and public health; therefore, better strategies are needed to mitigate the emergence of resistance. This study examined the expression of ARGs in Escherichia coli (E. coli) after exposure to sub-MIC (minimum inhibitory concentration) antibiotics for 15 days in the presence and absence of kaolinite. The results of the real-time polymerase chain reaction (PCR) showed that the expression levels of the eight target genes of E. coli adhering to kaolinite were relatively decreased, and the MIC results also indicated that the final resistance was lower than that of the strains without kaolinite. A close relationship between E. coli and kaolinite was also revealed, as well as a unique interfacial interaction. In addition, the differential protein expression was further analysed to detect proteins and genes associated with ARGs mutations, and then the underlying mechanisms of cell growth and metabolism were identified under low dose ampicillin stress to elucidate the role of kaolinite in the process. Molecular mechanisms analysis determined that when cells adhering to kaolinite were stressed, transport of ampicillin to the periplasmic space was reduced, and the redox metabolism of bacteria was promoted to combat the harsh environment. Moreover, cells synthesised related peptides or proteins under the action of ribosomal proteins to prevent toxic damage. Therefore, this work not only provides new insights into the cellular response to antibiotic stress, but also provides a topic for more research on methods to delay the emergence of ARGs.