ArticleJournal of thrombosis and haemostasis : JTH2017
Clumping factor A, von Willebrand factor-binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall.
Article in Journal of thrombosis and haemostasis : JTH, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Host-Bacterium Interaction Mechanisms inInternational journal of molecular sciences · 2023Pooled it
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- Dual-mode ClfA-targeting DARPin biologics protect against diverse methicillin-resistantbioRxiv : the preprint server for biology · 2026Article
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- Dual transcriptomic profiling ofmBio · 2025Article
- Pathogen virulence genes: Advances, challenges and future directions in infectious disease research (Review).International journal of molecular medicine · 2025Review
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- Cytokine-mediated inhibition of Staphylococcus aureus adherence and invasion into nonphagocytic cells.Medical microbiology and immunology · 2025Article
- Review
- Bloodstream infections: mechanisms of pathogenesis and opportunities for intervention.Nature reviews. Microbiology · 2025Review
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
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- Anti-Heliyon · 2024Article
- Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers.Pathogens (Basel, Switzerland) · 2024Review
- Vasculature-on-a-chip technologies as platforms for advanced studies of bacterial infections.Biomicrofluidics · 2024Review
- The role of human extracellular matrix proteins in defining Staphylococcus aureus biofilm infections.FEMS microbiology reviews · 2024Review
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- Protective Effect of Ticagrelor Against Infective Endocarditis Induced by VirulentJACC. Basic to translational science · 2023Article
- The Small Protein ScrA Influences Staphylococcus aureus Virulence-Related Processes via the SaeRS System.Microbiology spectrum · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Essentials Staphylococcus aureus (S. aureus) binds to endothelium via von Willebrand factor (VWF). Secreted VWF-binding protein (vWbp) mediates S. aureus adhesion to VWF under shear stress. vWbp interacts with VWF and the Sortase A-dependent surface protein Clumping factor A (ClfA). VWF-vWbp-ClfA anchor S. aureus to vascular endothelium under shear stress. SUMMARY: Objective When establishing endovascular infections, Staphylococcus aureus (S. aureus) overcomes shear forces of flowing blood by binding to von Willebrand factor (VWF). Staphylococcal VWF-binding protein (vWbp) interacts with VWF, but it is unknown how this secreted protein binds to the bacterial cell wall. We hypothesized that vWbp interacts with a staphylococcal surface protein, mediating the adhesion of S. aureus to VWF and vascular endothelium under shear stress. Methods We studied the binding of S. aureus to vWbp, VWF and endothelial cells in a micro-parallel flow chamber using various mutants deficient in Sortase A (SrtA) and SrtA-dependent surface proteins, and Lactococcus lactis expressing single staphylococcal surface proteins. In vivo adhesion of bacteria was evaluated in the murine mesenteric circulation using real-time intravital vascular microscopy. Results vWbp bridges the bacterial cell wall and VWF, allowing shear-resistant binding of S. aureus to inflamed or damaged endothelium. Absence of SrtA and Clumping factor A (ClfA) reduced adhesion of S. aureus to vWbp, VWF and activated endothelial cells. ADAMTS-13 and an anti-VWF A1 domain antibody, when combined, reduced S. aureus adhesion to activated endothelial cells by 90%. Selective overexpression of ClfA in the membrane of Lactococcus lactis enabled these bacteria to bind to VWF and activated endothelial cells but only in the presence of vWbp. Absence of ClfA abolished bacterial adhesion to the activated murine vessel wall. Conclusions vWbp interacts with VWF and with the SrtA-dependent staphylococcal surface protein ClfA. The complex formed by VWF, secreted vWbp and bacterial ClfA anchors S. aureus to vascular endothelium under shear stress.
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