ArticleJournal of innate immunity2012
Staphylococcus aureus virulence is enhanced by secreted factors that block innate immune defenses.
Article 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 31 papers.
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.
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Who cites it
31 citing papers in PubMed, 64 citations in OpenAlex.
- Complement inhibition by a unique cluster of immunomodulatory outer surface proteins of Borrelia recurrentis.Nature communications · 2026Article
- From Antibiotic Resistance to Bacterial Vaccines: A New Approach to Controlling Resistant Bacterial Infections.Infection and drug resistance · 2026Review
- The Epistemology of Bacterial Virulence Factor Characterization.Microorganisms · 2024Review
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- HowInternational journal of molecular sciences · 2023Review
- Article
- Extracellular fibrinogen-binding protein released by intracellular Staphylococcus aureus suppresses host immunity by targeting TRAF3.Nature communications · 2022Article
- CipA mediates complement resistance ofFrontiers in immunology · 2022Article
- Pathogenicity and virulence ofVirulence · 2021Review
- A Narrative Review on the Role ofOpen forum infectious diseases · 2021Review
- Review
- Selected Metabolites Profiling ofFrontiers in microbiology · 2020Article
- Immune Evasion byMicrobiology spectrum · 2019Review
- Whole-genome epidemiology, characterisation, and phylogenetic reconstruction of Staphylococcus aureus strains in a paediatric hospital.Genome medicine · 2018Article
- The transmembrane domain of the Staphylococcus aureus ESAT-6 component EssB mediates interaction with the integral membrane protein EsaA, facilitating partially regulated secretion in a heterologous host.Archives of microbiology · 2018Article
- An in vivo reporter assay for sRNA-directed gene control in Gram-positive bacteria: identifying a novel sRNA target in Staphylococcus aureus.Nucleic acids research · 2017Article
- Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria.PloS one · 2017Article
- Fibrinogen Is at the Interface of Host Defense and Pathogen Virulence in Staphylococcus aureus Infection.Seminars in thrombosis and hemostasis · 2016Review
- Exposure to TiO2 nanoparticles increases Staphylococcus aureus infection of HeLa cells.Journal of nanobiotechnology · 2016Article
- Extracellular Fibrinogen-binding Protein (Efb) from Staphylococcus aureus Inhibits the Formation of Platelet-Leukocyte Complexes.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 6 countries.
Funding
Abstract
Staphylococcus aureus is a leading human pathogen that causes a large variety of diseases. In vitro studies have shown that S. aureus secretes several small proteins that block specific elements of the host innate immune system, but their role in bacterial pathogenicity is unknown. For instance, the extracellular complement-binding protein (Ecb) impairs complement activation by binding to the C3d domain of C3. Its homolog, the extracellular fibrinogen-binding protein (Efb), is known to block both complement activation and neutrophil adhesion to fibrinogen. Here, we show that targeted inactivation of the genes encoding Ecb and Efb strongly attenuates S. aureus virulence in a murine infection model: mice experienced significantly higher mortality rates upon intravenous infection with wild-type bacteria (79%) than with an isogenic ΔEcbΔEfb mutant (21%). In addition, Ecb and Efb are both required for staphylococcal persistence in host tissues and abscess formation in the kidneys (27% for wild-type vs. 7% for the ΔEcbΔEfb mutant). During staphylococcal pneumonia, Ecb and Efb together promote bacterial survival in the lungs (p = 0.03) and block neutrophil influx into the lungs. Thus, Ecb and Efb are essential to S. aureus virulence in vivo and could be attractive targets in future vaccine development efforts.
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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.