ArticleJournal of advanced research2022
A vancomycin resistance-associated WalK(S221P) mutation attenuates the virulence of vancomycin-intermediate Staphylococcus aureus.
Article in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 32 citations in OpenAlex.
- Characterization and antibacterial efficacy of the broad-host-range phage P108 against biofilm-forming and methicillin-resistant Staphylococcus aureus.Virus research · 2026Article
- A Single Point Mutation in GraS Drives Co-Evolution of Vancomycin Resistance and Virulence inMicroorganisms · 2026Article
- Staphylococcal accessory regulator SarA-mediated modulation of autolysis and surface charge enablesmSystems · 2026Article
- Staphylococcus aureus sensor histidine kinase VraS mutations linked to antibiotic resistance affect enzymatic catalysis, stability, and substrate interactions.Archives of biochemistry and biophysics · 2026Article
- Histidinol dehydrogenase (HisD): a critical regulator ofMicrobiology spectrum · 2026Article
- CcpA promotesmLife · 2025Article
- Ultrahigh-throughput screening of heterogeneous vancomycin-intermediate Staphylococcus aureus based on fluorescence-activated droplet sorting.BMC medicine · 2025Article
- Treatment of Clinically Important Bacteria With Cold Atmospheric Plasma.Microbial biotechnology · 2025Review
- Genomic and phenotypic characterization of multidrug-resistantMicrobiology spectrum · 2025Article
- Beta-Lactam Antibiotics Promote Extracellular Vesicle Production of Staphylococcus aureus Through ROS-Mediated Lipid Metabolic Reprogramming.Journal of extracellular vesicles · 2025Article
- WalK(S221P) Mutation Promotes the Production ofMicroorganisms · 2025Article
- β-tricalcium phosphate/calcium sulfate loaded with contezolid acefosamil (MRX-4) for antimicrobial potency, prevention and killing efficacy of MRSA biofilm.Frontiers in pharmacology · 2025Article
- Trends and characteristics of multidrug-resistant MRSA in Norway 2008-2020.Frontiers in microbiology · 2025Article
- Vancomycin-Loaded Isogenous Membrane Vesicles for Macrophage Activation and Intracellular Methicillin-ResistantInternational journal of nanomedicine · 2025Article
- Homotypic Membrane Vesicle-Formulated VAN@Biomaterials research · 2025Article
- Alkaline shock protein 23 (Asp23)-controlled cell wall imbalance promotes membrane vesicle biogenesis in Staphylococcus aureus.Journal of extracellular vesicles · 2024Article
- Virulence attributes of successful methicillin-resistantClinical microbiology reviews · 2023Review
- Article
- Titanium-Dioxide-Nanoparticle-Embedded Polyelectrolyte Multilayer as an Osteoconductive and Antimicrobial Surface Coating.Materials (Basel, Switzerland) · 2023Article
- Bacterial-fungal interactions promote parallel evolution of global transcriptional regulators in a widespread Staphylococcus species.The ISME journal · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionVancomycin-intermediate Staphylococcus aureus (VISA) is typically associated with a decline in virulence. We previously reported a WalK(S221P) mutation that plays an important role in mediating vancomycin resistance in VISA XN108. Whether this mutation is implicated in bacterial virulence remains unknown.
objectivesThis study aimed to investigate the effect of WalK(S221P) mutation on the virulence of VISA and the underlying mechanism of this effect.
methodsThe influence of WalK(S221P) mutation on VISA virulence and its underlying mechanism were explored using animal models, RNA-seq analysis, RT-qPCR, hemolytic assay, slide coagulase test, Western blot, β-galactosidase assay, and electrophoresis mobility shift assay (EMSA).
resultsCompared with XN108, WalK(S221P)-reverted strain XN108-R exacerbated cutaneous infections with increased lesion size and extensive inflammatory infiltration in mouse models. The bacterial loads of S. aureus XN108-R in murine kidney increased compared with those of XN108. RNA-seq analysis showed upregulation of a set of virulence genes in XN108-R, which exhibited greater hemolytic and stronger coagulase activities compared with XN108. Introduction of WalK(S221P) to methicillin-resistant S. aureus USA300 and methicillin-susceptible strain Newman increased the vancomycin resistance of the mutants, which exhibited reduced hemolytic activities and decreased expression levels of many virulence factors compared with their progenitors. WalK(S221P) mutation weakened agr promoter-controlled β-galactosidase activity. EMSA results showed that WalK-phosphorylated WalR could directly bind to the agr promoter region, whereas WalK(S221P)-activated WalR reduced binding to the target promoter. Inactivation of agr in S. aureus did not affect their vancomycin susceptibility but mitigated the virulence alterations caused by WalK(S221P) mutation.
conclusionThe results of our study indicate that WalK(S221P) mutation can enhance vancomycin resistance in S. aureus of diverse genetic backgrounds. WalK(S221P)- bearing S. aureus strains exhibit reduced virulence. WalK(S221P) mutation may directly impair the activation of the agr system by WalR, thereby decreasing the expression of virulence factors in VISA.
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