Accelerated spread of antibiotic resistance genes (ARGs) induced by non-antibiotic conditions: Roles and mechanisms
- PMID: 36096030
- DOI: 10.1016/j.watres.2022.119060
Accelerated spread of antibiotic resistance genes (ARGs) induced by non-antibiotic conditions: Roles and mechanisms
Abstract
The global spread of antibiotic resistance genes (ARGs) has wreaked havoc with the treatment efficiency of antibiotics and, ultimately, anti-microbial chemotherapy, and has been conventionally attributed to the abuse and misuse of antibiotics. However, the ancient ARGs have alterative functions in bacterial physiology and thus they could be co-regulated by non-antibiotic conditions. Recent research has demonstrated that many non-antibiotic chemicals such as microplastics, metallic nanoparticles and non-antibiotic drugs, as well as some non-antibiotic conditions, can accelerate the dissemination of ARGs. These results suggested that the role of antibiotics might have been previously overestimated whereas the effects of non-antibiotic conditions were possibly ignored. Thus, in an attempt to fully understand the fate and behavior of ARGs in the eco-system, it is urgent to critically highlight the role and mechanisms of non-antibiotic chemicals and related environmental factors in the spread of ARGs. To this end, this timely review assessed the evolution of ARGs, especially its function alteration, summarized the non-antibiotic chemicals promoting the spread of ARGs, evaluated the non-antibiotic conditions related to ARG dissemination and analyzed the molecular mechanisms related to spread of ARGs induced by the non-antibiotic factors. Finally, this review then provided several critical perspectives for future research.
Keywords: Antibiotic resistance genes; Horizontal gene transfer; Mobile gene elements; Non-antibiotic chemicals; Vertical gene transfer.
Copyright © 2022 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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