ArticleInfection and immunity2016
Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Protective role of complement signaling in Kawasaki disease vasculitis.JCI insight · 2026Article
- Liver as a key organ for systemic antimicrobial defense.Hepatology communications · 2025Review
- Staphylococcus aureus thermonuclease NucA is a key virulence factor in septic arthritis.Communications biology · 2025Article
- Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis.JCI insight · 2025Article
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
- Identification of a genetic region linked to tolerance to MRSA infection using Collaborative Cross mice.PLoS genetics · 2024Article
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis.Communications biology · 2022Article
- Review
- Natural Human Immunity Against Staphylococcal Protein A Relies on Effector Functions Triggered by IgG3.Frontiers in immunology · 2022Article
- Commensal Bacteria AugmentFrontiers in cellular and infection microbiology · 2022Article
- Lipoteichoic Acid fromMicroorganisms · 2021Article
- Synovial Complement Factors in Patients with Periprosthetic Joint Infection after Undergoing Revision Arthroplasty of the Hip or Knee Joint.Diagnostics (Basel, Switzerland) · 2021Article
- Bacteria and Host Interplay inPathogens (Basel, Switzerland) · 2021Review
- Article
- Cell type specific gene expression profiling reveals a role for complement component C3 in neutrophil responses to tissue damage.Scientific reports · 2020Article
- Complement Receptor 3 Contributes to the Sexual Dimorphism in Neutrophil Killing ofJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Tofacitinib treatment aggravates Staphylococcus aureus septic arthritis, but attenuates sepsis and enterotoxin induced shock in mice.Scientific reports · 2020Article
- Protein profile of well-differentiated versus un-differentiated human bronchial/tracheal epithelial cells.Heliyon · 2020Article
- The role of Staphylococcus aureus lipoproteins in hematogenous septic arthritis.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system plays an essential role in the innate immune response and protection against bacterial infections. However, detailed knowledge regarding the role of complement in Staphylococcus aureus septic arthritis is still largely missing. In this study, we elucidated the roles of selected complement proteins in S. aureus septic arthritis. Mice lacking the complement component 3 (C3(-/-)), complement factor B (fB(-/-)), and receptor for C3-derived anaphylatoxin C3a (C3aR(-/-)) and wild-type (WT) control mice were intravenously or intra-articularly inoculated with S. aureus strain Newman. The clinical course of septic arthritis, as well as histopathological and radiological changes in joints, was assessed. After intravenous inoculation, arthritis severity and frequency were significantly higher in C3(-/-)mice than in WT controls, whereas fB(-/-)mice displayed intermediate arthritis severity and frequency. This was in accordance with both histopathological and radiological findings. C3, but not fB, deficiency was associated with greater weight loss, more frequent kidney abscesses, and higher bacterial burden in kidneys. S. aureus opsonized with C3(-/-)sera displayed decreased uptake by mouse peritoneal macrophages compared with bacteria opsonized with WT or fB(-/-)sera. C3aR deficiency had no effect on the course of hematogenous S. aureus septic arthritis. We conclude that C3 deficiency increases susceptibility to hematogenous S. aureus septic arthritis and impairs host bacterial clearance, conceivably due to diminished opsonization and phagocytosis of S. aureus.
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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.