ArticlePloS one2026
Induction of colistin resistance and environmental toxicity assessment in Escherichia coli.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The rise of Antimicrobial Resistance (AMR) among diverse microbial groups presents a growing threat to global public health. Colistin has become a last-line therapeutic option against multidrug-resistant Enterobacteriaceae. However, the global dissemination of mobile colistin resistance (mcr) genes, particularly in Escherichia coli, has raised significant concern. Among Gram-negatives, E. coli harbors the greatest diversity of mcr variants (mcr-1 to mcr-5), underscoring its importance as a model organism for resistance studies. This study investigated whether repeated exposure to subinhibitory concentrations of colistin sulfate could induce resistance in E. coli strain ATCC 25922. The strain was subjected to 10 growth cycles with 1.1 mg·L ⁻ ¹ of colistin, followed by one cycle at 6.4 mg·L ⁻ ¹. Minimum inhibitory concentrations (MICs) for colistin, ceftazidime, and gentamicin were determined, along with resistance maintenance assays and phenotypic evaluation of mcr-1 gene expression. All results were compared to a clinically isolated multidrug-resistant E. coli strain (CCBH 20178). Exposure to subinhibitory doses of colistin successfully induced resistance, with increased MIC values observed for colistin from 2 to 16mgL-1. Although resistance to ceftazidime and gentamicin was not established, a moderate elevation in ceftazidime MIC was noted, even after antibiotic withdrawal. Phenotypic expression of mcr-1 was detected in both the induced and clinical strains. Especially, the induced strain exhibited a two-fold increase in growth rate compared to susceptible control. These findings demonstrate that low-dose colistin exposure can promote the emergence of resistant E. coli strains and suggest a potential link between subinhibitory antimicrobial pressure and mcr-1-mediated resistance.
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