ArticlePloS one2026
Proteome-wide remodelling in Klebsiella pneumoniae during step-wise adaptive evolution against colistin.
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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Short-duration exposure (SDE) of antibiotics is among the major drivers of the emergence of antimicrobial resistance (AMR) among bacterial pathogens. Klebsiella pneumoniae is a critical priority bacterial pathogen and rapidly acquiring MDR/XDR traits even against major antibacterial classes of antibiotics. Since colistin is a last-resort antibiotic for treating drug-resistant K. pneumoniae infections and the development of new antibiotics is resource-intensive, understanding how antibiotic-resistance emerges following SDE is crucial for devising strategies to preserve antibiotics for future use. With this aim, we developed colistin (1x, 2x, and 4x MICs)-resistant K. pneumoniae using SDE of colistin and protein profiled to understand the emergence of SDE-induced colistin resistance. Interestingly, 1xMIC-adapted cells showed an ~ 8-fold increase in MIC for colistin, with no further rise at 2x or 4x MIC-adapted cells, indicating that the emergence of AMR can be a non-linear adaptive response and SDE of even 1x MIC-dose alone can trigger rapid physiological remodelling and target modification. Proteomic profiling identified 1379 proteins, including 245, 383, and 175 differentially expressed proteins (DEPs) in 1x, 2x, and 4x MIC-adapted cells, respectively. Among these, 75 DEPs were common across all conditions, representing a core proteomic signature consistently altered upon exposure and represented valS, arnA, arnB, pheT, and thrS the top upregulated proteins, and gjJ18, kphS, B5L96, potD, and phoU the top downregulated proteins. Functional enrichment highlighted catalytic, antioxidant, and binding activities, whereas protein-protein interaction (PPI) analysis revealed metabolic reprogramming, involving central carbon/amino acid metabolism and transcription/translation machinery associated with reduced antibiotic sensitivity. Lipopolysaccharide (LPS) modification (arnA, arnB, and phoU) and biomolecular synthesis (valS, pheT, and thrS) were the key functions altered during colistin adaptation. Since elevated arnA, arnB and phoU are known to reduce colistin binding to the bacterial surface, they may be facilitating the emergence of antibiotic resistance. Taken together, this research provides insight into SDE-induced colistin resistance in K. pneumoniae and may help to identify potential therapeutic and diagnostic interventions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.