ArticlePloS one2008
Fibrinogen binding sites P336 and Y338 of clumping factor A are crucial for Staphylococcus aureus virulence.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 67 citations in OpenAlex.
- Trial
- Safety and immunogenicity of an investigational 4-component Staphylococcus aureus vaccine with or without AS03B adjuvant: Results of a randomized phase I trial.Human vaccines & immunotherapeutics · 2015Trial
- Genetic determinants of Staphylococcus aureus adhesion shape virulence trade-offs in bacteremia.Nature communications · 2026Article
- Dual-mode ClfA-targeting DARPin biologics protect against diverse methicillin-resistantbioRxiv : the preprint server for biology · 2026Article
- Surface-Shaving ofMicroorganisms · 2024Article
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- Article
- Genome-wide association studies reveal candidate genes associated to bacteraemia caused by ST93-IV CA-MRSA.BMC genomics · 2021Article
- Multi-Antigen Outer Membrane Vesicle Engineering to Develop Polyvalent Vaccines: TheFrontiers in immunology · 2021Article
- In Vitro Assay for Quantifying Clumping of Staphylococcus aureus.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Article
- Surface Proteins ofMicrobiology spectrum · 2019Review
- Staphylococcus aureus adhesion in endovascular infections is controlled by the ArlRS-MgrA signaling cascade.PLoS pathogens · 2019Article
- Sortases, Surface Proteins, and Their Roles inMicrobiology spectrum · 2019Article
- Immunogenicity and protective efficacy of recombinant alkaline shock protein 23 fromCentral-European journal of immunology · 2018Article
- Adaptive Upregulation of Clumping Factor A (ClfA) by Staphylococcus aureus in the Obese, Type 2 Diabetic Host Mediates Increased Virulence.Infection and immunity · 2017Article
- Lessons from the Crystal Structure of the S. aureus Surface Protein Clumping Factor A in Complex With Tefibazumab, an Inhibiting Monoclonal Antibody.EBioMedicine · 2016Article
- Article
- Fibrinogen Is at the Interface of Host Defense and Pathogen Virulence in Staphylococcus aureus Infection.Seminars in thrombosis and hemostasis · 2016Review
- Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have earlier shown that clumping factor A (ClfA), a fibrinogen binding surface protein of Staphylococcus aureus, is an important virulence factor in septic arthritis. When two amino acids in the ClfA molecule, P(336) and Y(338), were changed to serine and alanine, respectively, the fibrinogen binding property was lost. ClfAP(336)Y(338) mutants have been constructed in two virulent S. aureus strains Newman and LS-1. The aim of this study was to analyze if these two amino acids which are vital for the fibrinogen binding of ClfA are of importance for the ability of S. aureus to generate disease. Septic arthritis or sepsis were induced in mice by intravenous inoculation of bacteria. The clfAP(336)Y(338) mutant induced significantly less arthritis than the wild type strain, both with respect to severity and frequency. The mutant infected mice developed also a much milder systemic inflammation, measured as lower mortality, weight loss, bacterial growth in kidneys and lower IL-6 levels. The data were verified with a second mutant where clfAP(336) and Y(338) were changed to alanine and serine respectively. When sepsis was induced by a larger bacterial inoculum, the clfAP(336)Y(338) mutants induced significantly less septic death. Importantly, immunization with the recombinant A domain of ClfAP(336)SY(338)A mutant but not with recombinant ClfA, protected against septic death. Our data strongly suggest that the fibrinogen binding activity of ClfA is crucial for the ability of S. aureus to provoke disease manifestations, and that the vaccine potential of recombinant ClfA is improved by removing its ability to bind fibrinogen.
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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.