ArticlePLoS pathogens2010
Staphylococcus aureus host cell invasion and virulence in sepsis is facilitated by the multiple repeats within FnBPA.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 154 citations in OpenAlex.
- Mast Cells in Host Defense Against Cutaneous Staphylococcus aureus Infection.Immunology and cell biology · 2026Review
- Osteomyelitis: Epidemiology, Classification, Pathophysiology, Clinical Features, Diagnosis, and Management.MedComm · 2026Review
- Genetic determinants of Staphylococcus aureus adhesion shape virulence trade-offs in bacteremia.Nature communications · 2026Article
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- Environmental cues in different host niches shape the survival fitness of Staphylococcus aureus.Nature communications · 2025Article
- Immune escape ofFrontiers in cellular and infection microbiology · 2025Review
- Research progress of implantable materials in antibacterial treatment of bone infection.Frontiers in bioengineering and biotechnology · 2025Review
- Elucidating the potential of isorhapontigenin in targeting the MgrA regulatory network: a paradigm shift for attenuating MRSA virulence.Antimicrobial agents and chemotherapy · 2024Article
- Activation of ARP2/3 and HSP70 Expression by Lipoteichoic Acid: Potential Bidirectional Regulation of Apoptosis in a Mastitis Inflammation Model.Biomolecules · 2024Article
- Prospects and challenges for the application of tissue engineering technologies in the treatment of bone infections.Bone research · 2024Review
- The phosphatidylinositol-5' phosphatase synaptojanin1 limits integrin-mediated invasion ofMicrobiology spectrum · 2024Article
- Staphylococcus aureus Panton-Valentine Leukocidin worsens acute implant-associated osteomyelitis in humanized BRGSF mice.JBMR plus · 2024Article
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- Repurposing Inhibitors of Phosphoinositide 3-kinase as Adjuvant Therapeutics for Bacterial Infections.Frontiers in antibiotics · 2023Article
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- In Silico Genome-Scale Analysis of Molecular Mechanisms Contributing to the Development of a Persistent Infection with Methicillin-ResistantInternational journal of molecular sciences · 2022Article
- Skeletal infections: microbial pathogenesis, immunity and clinical management.Nature reviews. Microbiology · 2022Review
- Host-pathogen interactions of clinicalVirulence · 2021Article
- Emergence of a mupirocin-resistant, methicillin-susceptible Staphylococcus aureus clone associated with skin and soft tissue infections in Greece.BMC microbiology · 2021Article
- Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus.Scientific reports · 2021Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Entry of Staphylococcus aureus into the bloodstream can lead to metastatic abscess formation and infective endocarditis. Crucial to the development of both these conditions is the interaction of S. aureus with endothelial cells. In vivo and in vitro studies have shown that the staphylococcal invasin FnBPA triggers bacterial invasion of endothelial cells via a process that involves fibronectin (Fn) bridging to alpha(5)beta(1) integrins. The Fn-binding region of FnBPA usually contains 11 non-identical repeats (FnBRs) with differing affinities for Fn, which facilitate the binding of multiple Fn molecules and may promote integrin clustering. We thus hypothesized that multiple repeats are necessary to trigger the invasion of endothelial cells by S. aureus. To test this we constructed variants of fnbA containing various combinations of FnBRs. In vitro assays revealed that endothelial cell invasion can be facilitated by a single high-affinity, but not low-affinity FnBR. Studies using a nisin-inducible system that controlled surface expression of FnBPA revealed that variants encoding fewer FnBRs required higher levels of surface expression to mediate invasion. High expression levels of FnBPA bearing a single low affinity FnBR bound Fn but did not invade, suggesting that FnBPA affinity for Fn is crucial for triggering internalization. In addition, multiple FnBRs increased the speed of internalization, as did higher expression levels of FnBPA, without altering the uptake mechanism. The relevance of these findings to pathogenesis was demonstrated using a murine sepsis model, which showed that multiple FnBRs were required for virulence. In conclusion, multiple FnBRs within FnBPA facilitate efficient Fn adhesion, trigger rapid bacterial uptake and are required for pathogenesis.
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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.