ArticleInfection and drug resistance2026
Integrated Proteomics and Metabolomics Reveal Multifaceted Mechanisms of Colistin Resistance in
Article in Infection and drug resistance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The emergence of colistin-resistant Methods: This study utilized integrated tandem mass tag (TMT)-based proteomics and untargeted metabolomics to compare a representative drug-sensitive (DS) strain, a colistin-sensitive multidrug-resistant (MDR-CRAB) strain, and a colistin-resistant extensively drug-resistant (XDR-CRAB) isolate from a Guangzhou hospital, China, with a primary focus on the molecular features associated with resistance in the XDR isolate. Results: Proteomic analysis identified 260 differentially expressed proteins (DEPs) across these strains, with 98 strongly linked to the colistin-resistant phenotype. These DEPs were enriched in functions related to polysaccharide and sulfate transport, aromatic compound degradation, and cationic antimicrobial peptide (CAMP) resistance. Upregulation of the lipid A modification system, driven by increased expression of PmrA (4.2-fold), PmrB (2.9-fold), and PmrC (5.5-fold) in the XDR strain compared to the MDR strain, is consistent with this CAMP resistance. Metabolomic analysis identified 747 metabolites, with lipids and lipid-like molecules being the most altered class. The XDR strain exhibited reduced relative abundance of several glycerophospholipids and fatty acids/conjugates, when compared to the MDR strain, indicating cell membrane remodeling. Pathway enrichment analysis further implicated purine, glycerophospholipid, starch/sucrose, and glutathione metabolism in colistin resistance. Conclusion: Colistin resistance in
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