ABSTRACT
Antibiotic resistance poses a major threat to public health. Overuse and misuse of antibiotics are generally recognised 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-lactamase and multi-drug efflux pump, 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 highlights the need for controlling biocide applications.
ABBREVIATIONS
- NAAM
- non-antibiotic, anti-microbial
- TCS
- triclosan
- MIC
- minimum inhibition concentration
- ROS
- Reactive Oxidative Species
- SIM
- stress-induced mutagenesis
- AMX
- amoxicillin
- LEX
- cephalexin
- TET
- tetracycline
- CHL
- chloramphenicol
- LVX
- levofloxacin
- NOR
- norfloxacin
- KAN
- Kanamycin
- AMP
- ampicillin
- DCF-DA
- 2’,7’-dichlorofluorescein diacetate
- TBHP
- N,N-dialkylanilines with tert-butyl hydroperoxide
- SNP
- single nucleotide polymorphism
- FDR
- false discovery rate
- FPKM
- fragments per kilobase of a gene per million mapped reads
- LFC
- log2 fold change