Antibiotic resistance poses a major threat to public health. Overuse and misuse of antibiotics are generally recognized as the key factors contributing to antibiotic resistance. However, whether non-antibiotic, anti-microbial (NAAM) chemicals can directly induce antibiotic resistance is unclear. We aim to investigate whether the exposure to a NAAM chemical triclosan (TCS) has an impact on inducing antibiotic resistance on Escherichia coli. Here, we report that at a concentration of 0.2 mg/L TCS induces multi-drug resistance in wild-type Escherichia coli after 30-day TCS exposure. The oxidative stress induced by TCS caused genetic mutations in genes such as fabI, frdD, marR, acrR and soxR, and subsequent up-regulation of the transcription of genes encoding beta-lactamases and multi-drug efflux pumps, together with down-regulation of genes related to membrane permeability. The findings advance our understanding of the potential role of NAAM chemicals in the dissemination of antibiotic resistance in microbes, and highlight the need for controlling biocide applications.

抗生素耐药性对公共健康构成重大威胁。普遍认为，抗生素的过度使用和滥用是导致抗生素耐药性的关键因素。但是，尚不清楚非抗生素，抗微生物（NAAM）化学药品能否直接诱导抗生素耐药性。我们的目标是调查暴露于化学NAAM三氯生（TCS）是否对诱导耐药性产生影响大肠埃希氏大肠杆菌。在这里，我们报道在30天的TCS暴露后，浓度为0.2 mg / L的TCS会在野生型大肠杆菌中诱导多药耐药性。TCS诱导的氧化应激导致fabI，frdD，marR，acrR等基因的遗传突变和soxR ，以及随后上调编码β-内酰胺酶和多药外排泵的基因的转录，以及与膜通透性相关的基因的下调。这些发现提高了我们对NAAM化学品在微生物中耐药性传播中潜在作用的理解，并强调了控制杀生物剂应用的必要性。