ReviewJournal of innate immunity2012
Staphylococcus aureus secretes coagulase and von Willebrand factor binding protein to modify the coagulation cascade and establish host infections.
Review in Journal of innate immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Host-Bacterium Interaction Mechanisms inInternational journal of molecular sciences · 2023Pooled it
- Aberrant stromal tissue factor localisation and mycolactone-driven vascular dysfunction, exacerbated by IL-1β, are linked to fibrin formation in Buruli ulcer lesions.PLoS pathogens · 2022Trial
- Molecular basis and therapeutic potential of sortase A inhibitors as new antibiotics against MDR pathogens.Open biology · 2026Review
- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- Osteomyelitis.Nature reviews. Disease primers · 2026Review
- Smartphone-based multispectral autofluorescence analysis of bacteria mixtures of staphylococci using convolutional neural network.Journal of biological engineering · 2026Article
- Fibrin barriers limit vancomycin penetration into staphylococcal abscess communities and maintainbioRxiv : the preprint server for biology · 2026Article
- Staphylococcal phages as agents of evolution and innovation: From gene flow to next-generation therapeutics.Genetics and molecular biology · 2026Article
- Insights from the Evolution of Coagulation: A New Perspective on Anti-Inflammatory Strategies in the ICU-Focus on the Contact Activation System.Biomedicines · 2025Review
- Bacterial infection and activation of the contact pathway of coagulation.Blood vessels, thrombosis & hemostasis · 2025Review
- Article
- Culture-free detection of bacteria from blood for rapid sepsis diagnosis.NPJ digital medicine · 2025Article
- Immune dysfunction during S. aureus biofilm-associated implant infections: opportunities for novel therapeutic strategies.NPJ biofilms and microbiomes · 2025Review
- Factor XII-driven coagulation traps bacterial infections.The Journal of experimental medicine · 2025Article
- Potential Compounds as Inhibitors of Staphylococcal Virulence Factors Involved in the Development of Thrombosis.Toxins · 2025Review
- Review
- DisarmingPathogens (Basel, Switzerland) · 2025Review
- Spin polarization induced by atomic strain of MBene promotes the ·ONature communications · 2025Article
- Rhizosphere-derivedFrontiers in plant science · 2025Article
- Speckle fluctuations reveal dynamics of microparticles in fibrin scaffolds in a model of bacterial infection.npj biological physics and mechanics · 2025Article
28 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Clinical isolates of Staphylococcus aureus secrete coagulases, polypeptides that bind to and activate prothrombin, thereby converting fibrinogen to fibrin and promoting the clotting of plasma or blood. Two staphylococcal products, the canonical coagulase (Coa) as well as the recently identified von Willebrand factor binding protein (vWbp), promote similar modifications of the coagulation cascade during host infection. Staphylococcal binding to fibrinogen or fibrin is an important attribute of disease pathogenesis, which leads to the formation of abscesses and bacterial persistence in host tissues and also enables the pathogen to cause lethal sepsis. Circumstantial evidence suggests that the product of coagulase activity, staphylococci captured within a fibrin meshwork, enable this pathogen to disseminate as thromboembolic lesions and to resist opsonophagocytic clearance by host immune cells. In addition, the coagulation products of staphylococci appear to display discrete differences when compared to those of thrombin-mediated coagulation, the latter representing a key innate defense mechanism against many invading pathogens. Preclinical evidence suggests that inactivation or neutralization of coagulases may prevent the pathogenesis of staphylococcal infections, a strategy that could be used to combat the current epidemic of hospital-acquired infections with drug-resistant S. aureus isolates.
Indexed as
Identifiers
What OpenQuestion holds
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.