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Colistin resistance plasmids dually enhance bacterial virulence and antibiotic resistance via surface polysaccharide

Eunbyeol Ahn1,2,3, Jinshil Kim1,3,4,5, Junyao Jiang6

  • 1Department of Food and Animal Biotechnology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea.

Nature Communications
|November 12, 2025
PubMed

Insights

The mobilized colistin-resistance gene (mcr-1) plasmid enhances Escherichia coli pathogenicity and colistin resistance by regulating surface polysaccharide production. This highlights how resistance genes can unexpectedly increase bacterial virulence.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • The prevalence of colistin-resistance gene (mcr-1) plasmids in multidrug-resistant Gram-negative bacteria is high.
  • The impact of mcr-1 plasmids on bacterial physiology and virulence is not fully understood.

Purpose of the Study:

  • To investigate how mcr-1 plasmids affect bacterial physiology and virulence.
  • To elucidate the mechanism by which mcr-1 plasmids enhance pathogenicity in Escherichia coli.

Main Methods:

  • Plasmid acquisition experiments in Escherichia coli.
  • Analysis of gene regulation (wec operon) and surface polysaccharide biosynthesis.
  • Murine model for virulence assessment.
  • Genomic analysis of mcr plasmids.

Main Results:

  • mcr-1 plasmid acquisition increased both antimicrobial resistance and pathogenicity in Escherichia coli.
  • The transcriptional regulator EcaR and MCR-1 cooperate to activate the wec operon, driving enterobacterial common antigen (ECA) and O-chain polysaccharide synthesis.
  • These polysaccharides enhance bile resistance and virulence, and further increase colistin resistance.
  • Genomic analysis revealed co-occurrence of mcr-1 and ecaR on common plasmid types (IncI2, IncX4).

Conclusions:

  • mcr-1 plasmids can remodel the bacterial surface by coordinating resistance and virulence gene expression.
  • Horizontal gene transfer of mcr-1 plasmids can lead to increased bacterial pathogenicity.
  • The findings reveal a mechanism linking antimicrobial resistance and virulence through plasmid-mediated regulation of surface polysaccharides.

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