ArticleClinical proteomics2026
Distinct proteomic profiles of clinical isolates show diversity of Pseudomonas aeruginosa colistin-resistance.
Article in Clinical proteomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
- Clinical and Epidemiological Landscape of Antimicrobial Resistance and Virulence inAntibiotics (Basel, Switzerland) · 2026Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPseudomonas aeruginosa is a multidrug-resistant pathogenic bacterium that poses a substantial threat to global public health because of its resistance to antibiotics, and especially to last-resort colistin. The aim of this study is to perform a comparative analysis between the antibiotic-sensitive isolate A and the resistant isolate C (8 µg/mL for isolate A and 128 µg/mL for isolate C), with the intent of elucidating the discrete molecular mechanisms underpinning resistance. This investigation seeks to distinguish between pathways inherently expressed in the absence of antibiotic exposure (acquired resistance) and those activated in response to antibiotic challenge (induced resistance), thereby providing deeper insights into the multifaceted nature of antimicrobial resistance in P. aeruginosa.
resultsProteomic analysis, performed under basal conditions and after exposure to increasing doses of colistin, revealed that, although both isolates have intrinsic resistance to several antimicrobials, the mechanisms underlying colistin resistance diverge significantly. While isolate A showed a stable proteomic response, characterized by the overexpression of proteins related to membrane remodeling and efflux systems, isolate C demonstrated a more dynamic response, evidenced by metabolic adaptations and oxidative stress mitigation mechanisms. These differences suggest that each isolate employs specific strategies to cope with antimicrobial pressure, which has direct implications for the choice of alternative therapies and the development of optimized dosing regimens.
conclusionsThe findings have direct implications for the choice of alternative therapies and the development of optimized dosing regimen. In summary, the results reinforce the complexity of resistance mechanisms in P. aeruginosa and highlight the importance of personalized therapeutic approaches for the management of infections caused by multidrug-resistant isolates.
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