ArticlePloS one2012
Staphylococcus aureus proteins Sbi and Efb recruit human plasmin to degrade complement C3 and C3b.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Emerging threats and zoonotic implications of antibiotic-resistant Staphylococcus spp. in domesticated cats: a review.Antonie van Leeuwenhoek · 2026Review
- Complement inhibition by a unique cluster of immunomodulatory outer surface proteins of Borrelia recurrentis.Nature communications · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Linking Virulence and Iron Limitation Response inJournal of proteome research · 2025Article
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- HylS', a fragment of truncated hyaluronidase ofVirulence · 2024Article
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Clonal Diversity, Antibiotic Resistance, and Virulence Factor Prevalence of Community AssociatedPathogens (Basel, Switzerland) · 2023Article
- Roles of the Crp/Fnr Family Regulator ArcR in the Hemolysis and Biofilm ofMicroorganisms · 2023Article
- In Silico Genome-Scale Analysis of Molecular Mechanisms Contributing to the Development of a Persistent Infection with Methicillin-ResistantInternational journal of molecular sciences · 2022Article
- Immunomodulatory Role ofPathogens (Basel, Switzerland) · 2022Review
- The Protease SplB of Staphylococcus aureus Targets Host Complement Components and Inhibits Complement-Mediated Bacterial Opsonophagocytosis.Journal of bacteriology · 2022Article
- A General Map of Transcriptional Expression of Virulence, Metabolism, and Biofilm Formation Adaptive Changes ofFrontiers in microbiology · 2022Article
- Interaction between Borrelia miyamotoi variable major proteins Vlp15/16 and Vlp18 with plasminogen and complement.Scientific reports · 2021Article
- ApoE attenuates unresolvable inflammation by complex formation with activated C1q.Nature medicine · 2019Article
- Staphylococcus pseudintermedius Sbi paralogs inhibit complement and bind IgM, IgG Fc and Fab.PloS one · 2019Article
- Survival of Staphylococcus epidermidis in Fibroblasts and Osteoblasts.Infection and immunity · 2018Article
- Article
- Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria.PloS one · 2017Article
- Molecular Interactions of Human Plasminogen with Fibronectin-binding Protein B (FnBPB), a Fibrinogen/Fibronectin-binding Protein from Staphylococcus aureus.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon host infection, the human pathogenic microbe Staphylococcus aureus (S. aureus) immediately faces innate immune reactions such as the activated complement system. Here, a novel innate immune evasion strategy of S. aureus is described. The staphylococcal proteins surface immunoglobulin-binding protein (Sbi) and extracellular fibrinogen-binding protein (Efb) bind C3/C3b simultaneously with plasminogen. Bound plasminogen is converted by bacterial activator staphylokinase or by host-specific urokinase-type plasminogen activator to plasmin, which in turn leads to degradation of complement C3 and C3b. Efb and to a lesser extend Sbi enhance plasmin cleavage of C3/C3b, an effect which is explained by a conformational change in C3/C3b induced by Sbi and Efb. Furthermore, bound plasmin also degrades C3a, which exerts anaphylatoxic and antimicrobial activities. Thus, S. aureus Sbi and Efb comprise platforms to recruit plasmin(ogen) together with C3 and its activation product C3b for efficient degradation of these complement components in the local microbial environment and to protect S. aureus from host innate immune reactions.
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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.