Related Experiment Video
Updated: Jul 28, 2026

Purification and Visualization of Lipopolysaccharide from Gram-negative Bacteria by Hot Aqueous-phenol Extraction
Published on: May 28, 2012
Structural Modification of Lipopolysaccharide Conferred by mcr-1 in Gram-Negative ESKAPE Pathogens
Yi-Yun Liu1,2, Courtney E Chandler3, Lisa M Leung3
1Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Abstract:
mcr-1 was initially reported as the first plasmid-mediated colistin resistance gene in clinical isolates of Escherichia coli and Klebsiella pneumoniae in China and has subsequently been identified worldwide in various species of the family Enterobacteriaceaemcr-1 encodes a phosphoethanolamine transferase, and its expression has been shown to generate phosphoethanolamine-modified bis-phosphorylated hexa-acylated lipid A in E. coli Here, we investigated the effects of mcr-1 on colistin susceptibility and on lipopolysaccharide structures in laboratory and clinical strains of the Gram-negative ESKAPE (Enterococcus faecium, Staphylococcus aureus, K. pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens, which are often treated clinically by colistin. The effects of mcr-1 on colistin resistance were determined using MIC assays of laboratory and clinical strains of E. coli, K. pneumoniae, A. baumannii, and P. aeruginosa Lipid A structural changes resulting from MCR-1 were analyzed by mass spectrometry. The introduction of mcr-1 led to colistin resistance in E. coli, K. pneumoniae, and A. baumannii but only moderately reduced susceptibility in P. aeruginosa Phosphoethanolamine modification of lipid A was observed consistently for all four species. These findings highlight the risk of colistin resistance as a consequence of mcr-1 expression among ESKAPE pathogens, especially in K. pneumoniae and A. baumannii Furthermore, the observation that lipid A structures were modified despite only modest increases in colistin MICs in some instances suggests more sophisticated surveillance methods may need to be developed to track the dissemination of mcr-1 or plasmid-mediated phosphoethanolamine transferases in general.
Insights
The mcr-1 gene confers colistin resistance in key Gram-negative pathogens like E. coli and K. pneumoniae by altering lipid A structures. This necessitates enhanced surveillance for tracking resistance gene spread.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- The mcr-1 gene, encoding a phosphoethanolamine transferase, is the first identified plasmid-mediated colistin resistance gene.
- It has been detected globally in Enterobacteriaceae, posing a significant threat to public health.
- Colistin is a critical last-resort antibiotic for treating infections caused by multidrug-resistant Gram-negative bacteria.
Purpose of the Study:
- To investigate the impact of mcr-1 on colistin susceptibility in ESKAPE pathogens.
- To analyze the structural modifications of lipopolysaccharide (LPS) in response to mcr-1 expression.
- To assess the risk of colistin resistance mediated by mcr-1 in clinically relevant bacteria.
Main Methods:
- Minimum Inhibitory Concentration (MIC) assays were performed on laboratory and clinical strains of Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii, and Pseudomonas aeruginosa.
- Lipid A structures were analyzed using mass spectrometry to detect modifications induced by MCR-1.
- The presence and effects of mcr-1 were evaluated across different Gram-negative ESKAPE pathogens.
Main Results:
- Introduction of mcr-1 resulted in significant colistin resistance in E. coli, K. pneumoniae, and A. baumannii.
- A moderate reduction in colistin susceptibility was observed in P. aeruginosa.
- Consistent phosphoethanolamine modification of lipid A was detected in all tested species, regardless of the degree of resistance.
Conclusions:
- mcr-1 expression poses a substantial risk for colistin resistance development in ESKAPE pathogens, particularly K. pneumoniae and A. baumannii.
- Lipid A modification by MCR-1 can occur even with modest increases in colistin MICs.
- Advanced surveillance strategies are crucial for monitoring the dissemination of mcr-1 and similar resistance mechanisms.
More Related Videos
12:57Isolation and Chemical Characterization of Lipid A from Gram-negative Bacteria
Published on: September 16, 2013
10:24Separation of the Cell Envelope for Gram-negative Bacteria into Inner and Outer Membrane Fractions with Technical Adjustments for Acinetobacter baumannii
Published on: April 10, 2020
Related Concept Videos
Formation of Lipopolysaccharides
Archaeal Cell Wall
Regulation of Bacterial Virulence
Mechanism of Antibiotic Resistance in MRSA
Inhibitors of Gram-positive Cell Wall Synthesis
Clinical Significance of Antibiotic Resistance