ArticlePLoS pathogens2013
Phagocytosis escape by a Staphylococcus aureus protein that connects complement and coagulation proteins at the bacterial surface.
Article in PLoS pathogens, 2013. 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, 134 citations in OpenAlex.
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- Bacterial interactions with platelets: defining key themes.Frontiers in immunology · 2025Review
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- Staphylococcus aureus SaeRS impairs macrophage immune functions through bacterial clumps formation in the early stage of infection.NPJ biofilms and microbiomes · 2024Article
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- The Epistemology of Bacterial Virulence Factor Characterization.Microorganisms · 2024Review
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Transcriptomic analysis of lipoteichoic acid‑treated undifferentiated and neutrophil‑like differentiated HL‑60 cells.Experimental and therapeutic medicine · 2024Article
- Fibrinogen induces inflammatory responses via the immune activating receptor LILRA2.Frontiers in immunology · 2024Article
- Secretory IgA impacts the microbiota density in the human nose.Microbiome · 2023Article
- Fibrinogen γ' promotes host survival during Staphylococcus aureus septicemia in mice.Journal of thrombosis and haemostasis : JTH · 2023Article
- A Comprehensive Review on the Roles of Metals Mediating Insect-Microbial Pathogen Interactions.Metabolites · 2023Review
- GFP fusions of Sec-routed extracellular proteins inMicrobial cell (Graz, Austria) · 2023Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Upon contact with human plasma, bacteria are rapidly recognized by the complement system that labels their surface for uptake and clearance by phagocytic cells. Staphylococcus aureus secretes the 16 kD Extracellular fibrinogen binding protein (Efb) that binds two different plasma proteins using separate domains: the Efb N-terminus binds to fibrinogen, while the C-terminus binds complement C3. In this study, we show that Efb blocks phagocytosis of S. aureus by human neutrophils. In vitro, we demonstrate that Efb blocks phagocytosis in plasma and in human whole blood. Using a mouse peritonitis model we show that Efb effectively blocks phagocytosis in vivo, either as a purified protein or when produced endogenously by S. aureus. Mutational analysis revealed that Efb requires both its fibrinogen and complement binding residues for phagocytic escape. Using confocal and transmission electron microscopy we show that Efb attracts fibrinogen to the surface of complement-labeled S. aureus generating a 'capsule'-like shield. This thick layer of fibrinogen shields both surface-bound C3b and antibodies from recognition by phagocytic receptors. This information is critical for future vaccination attempts, since opsonizing antibodies may not function in the presence of Efb. Altogether we discover that Efb from S. aureus uniquely escapes phagocytosis by forming a bridge between a complement and coagulation protein.
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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.