ArticleInfection and immunity2010
Clumping factor A interaction with complement factor I increases C3b cleavage on the bacterial surface of Staphylococcus aureus and decreases complement-mediated phagocytosis.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
59 citing papers in PubMed, 119 citations in OpenAlex.
- Dual-mode ClfA-targeting DARPin biologics protect against diverse methicillin-resistantbioRxiv : the preprint server for biology · 2026Article
- Rapid Detection ofBiosensors · 2025Article
- Article
- Structure of ClfA002 in Complex With Neutralizing Antibody AZD7745 Provides Insight into Its Broad Neutralization Mechanism in Staphylococcus aureus Infection.The Journal of infectious diseases · 2025Article
- Biofilm Formation, c-di-GMP Production, and Antimicrobial Resistance in Staphylococcal Strains Isolated from Prosthetic Joint Infections: A Pilot Study in Total Hip and Knee Arthroplasty Patients.International journal of molecular sciences · 2025Article
- A surface lipoprotein on Pasteurella multocida binds complement factor I to promote immune evasion.PLoS pathogens · 2025Article
- Genome-based model for differentiating between infection and carriageMicrobiology spectrum · 2024Article
- Genomic analysis ofiScience · 2024Article
- Clonal Diversity, Antibiotic Resistance, and Virulence Factor Prevalence of Community AssociatedPathogens (Basel, Switzerland) · 2023Article
- Fibrinogen γ' promotes host survival during Staphylococcus aureus septicemia in mice.Journal of thrombosis and haemostasis : JTH · 2023Article
- Virulence genes and antibiotic resistance profiles ofIranian journal of veterinary research · 2023Article
- Adhesive Virulence Factors ofACS bio & med chem Au · 2022Article
- Diversity and pathogenesis of Staphylococcus aureus from bovine mastitis: current understanding and future perspectives.BMC veterinary research · 2022Review
- CipA mediates complement resistance ofFrontiers in immunology · 2022Article
- The N2N3 domains of ClfA, FnbpA and FnbpB in Staphylococcus aureus bind to human complement factor H, and their antibodies enhance the bactericidal capability of human blood.Journal of biochemistry · 2021Article
- Bacteria and Host Interplay inPathogens (Basel, Switzerland) · 2021Review
- The Recombinant Expression Proteins FnBP and ClfA FromFrontiers in veterinary science · 2021Article
- The iron-regulated surface determinant B (IsdB) protein fromThe Journal of biological chemistry · 2020Article
- Surface Proteins ofMicrobiology spectrum · 2019Review
- Immune Evasion byMicrobiology spectrum · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human complement system is important in the immunological control of Staphylococcus aureus infection. We showed previously that S. aureus surface protein clumping factor A (ClfA), when expressed in recombinant form, bound complement control protein factor I and increased factor I cleavage of C3b to iC3b. In the present study, we show that, compared to the results for the wild type, when isogenic ClfA-deficient S. aureus mutants were incubated in serum, they bound less factor I, generated less iC3b on the bacterial surface, and bound fewer C3 fragments. It has been shown previously that two amino acids in ClfA (P(336) and Y(338)) are essential for fibrinogen binding. However, S. aureus expressing ClfA(P336A Y338S) was less virulent than ClfA-deficient strains in animal models. This suggested that ClfA contributed to S. aureus virulence by a mechanism different than fibrinogen binding. In the present study, we showed that S. aureus expressing ClfA(P336A Y338S) was more susceptible to complement-mediated phagocytosis than a ClfA-null mutant or the wild type. Unlike ClfA, ClfA(P336A Y338S) did not enhance factor I cleavage of C3b to iC3b and inhibited the cofactor function of factor H. Fibrinogen enhanced factor I binding to ClfA and the S. aureus surface. Twenty clinical S. aureus strains all expressed ClfA and bound factor I. High levels of factor I binding by clinical strains correlated with poor phagocytosis. In summary, our results suggest that the interaction of ClfA with factor I contributes to S. aureus virulence by a complement-mediated mechanism.
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.