ArticleJournal of biomedical science2023
Reduced virulence in tigecycline-resistant Klebsiella pneumoniae caused by overexpression of ompR and down-regulation of ompK35.
Article in Journal of biomedical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Post-infection colonization and recurrent infections by ST11-KL64 carbapenem-resistantVirulence · 2026Article
- Molecular epidemiology of levofloxacin-resistantMicrobiology spectrum · 2026Article
- The EnvZ/OmpR two-component regulatory system regulates biofilm formation inFrontiers in microbiology · 2026Article
- Molecular epidemiology and clinical characteristics of carbapenem-resistantMicrobiology spectrum · 2025Article
- Effect of colistin-tigecycline combination on colistin-resistant and carbapenem-resistantMicrobiology spectrum · 2025Article
- Exploring current hypervirulentFrontiers in microbiology · 2025Review
- Extended-Spectrum β-Lactamase-ProducingInfection and drug resistance · 2025Article
- Third-Generation Tetracyclines: Current Knowledge and Therapeutic Potential.Biomolecules · 2024Review
- Evaluation of Antibiotic Resistance Mechanisms in Gram-Negative Bacteria.Antibiotics (Basel, Switzerland) · 2023Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe development of tigecycline resistance in hypervirulent Klebsiella pneumoniae strains has resulted in decreased virulence that is associated with reduced production of capsular polysaccharides (CPS). In this study, we investigated the mechanisms that link tigecycline susceptibility to decreased virulence.
methodsWe compared transcriptomes from tigecycline-susceptible wild-type strains and tigecycline-resistant mutants using mRNA sequencing. ompR-overexpressed and ompR-deleted mutants were constructed from wild-type strains and tigecycline-resistant mutants, respectively. Antibiotic susceptibility tests were performed, and string tests and precipitation assays were conducted to identify phenotypic changes related to tigecycline susceptibility and ompR expression. Bacterial virulence was assessed by serum resistance and Galleria mellonella infection assays.
resultsTranscriptomic analyses demonstrated a significant decrease in the expression of ompK35 in the tigecycline-resistant mutants. We observed that tigecycline-resistant mutants overexpressed ompR, and that the expression of ompK35 was regulated negatively by ompR. While tigecycline-resistant mutants and ompR-overexpressed mutants exhibited reduced hypermucoviscosity and virulence, deletion of ompR from tigecycline-resistant mutants restored their hypermucoviscosity and virulence.
conclusionsIn hypervirulent K. pneumoniae strains, ompR expression, which is regulated by exposure to tigecycline, may affect the production of CPS, leading to bacterial virulence.
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