ArticlePloS one2017
Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- The Complement System in the Setting of Critical Illness-A Narrative Review.Biomolecules · 2026Review
- The Pathogenicity Mechanisms ofInternational journal of molecular sciences · 2025Review
- Linking Virulence and Iron Limitation Response inJournal of proteome research · 2025Article
- Article
- Combating multidrug-resistant (MDR) Staphylococcus aureus infection using terpene and its derivative.World journal of microbiology & biotechnology · 2024Review
- Clonal Diversity, Antibiotic Resistance, and Virulence Factor Prevalence of Community AssociatedPathogens (Basel, Switzerland) · 2023Article
- Molecular Mechanisms of Drug Resistance inInternational journal of molecular sciences · 2022Review
- A small regulatory RNA alters Staphylococcus aureus virulence by titrating RNAIII activity.Nucleic acids research · 2021Article
- Article
- Complement Evasion Strategies of Human Pathogenic Bacteria.Indian journal of microbiology · 2020Review
- Monocytes Undergo Functional Reprogramming to Generate Immunosuppression through HIF-1Mediators of inflammation · 2020Article
- Mechanistic Understanding of Cell Recognition and Immune Reaction via CR1/CR3 by HAP- and SiOBioMed research international · 2020Article
- Function and Dysfunction of Complement Factor H During Formation of Lipid-Rich Deposits.Frontiers in immunology · 2020Review
- The Role of Macrophages inFrontiers in immunology · 2020Review
- Development of a vaccine against Staphylococcus aureus invasive infections: Evidence based on human immunity, genetics and bacterial evasion mechanisms.FEMS microbiology reviews · 2020Review
- Staphylococcus aureus toxin LukSF dissociates from its membrane receptor target to enable renewed ligand sequestration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Complement Factor H and Apolipoprotein E Participate in Regulation of Inflammation in THP-1 Macrophages.Frontiers in immunology · 2018Article
- Increase in complement iC3b is associated with anti-inflammatory cytokine expression during late pregnancy in mice.PloS one · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphyloccus aureus is a major human pathogen leading frequently to sepsis and soft tissue infections with abscesses. Multiple virulence factors including several immune modulating molecules contribute to its survival in the host. When S. aureus invades the human body, one of the first line defenses is the complement system, which opsonizes the bacteria with C3b and attract neutrophils by release of chemotactic peptides. Neutrophils express Complement receptor-1 [CR1, CD35) that interacts with the C3b-opsonized particles and thereby plays an important role in pathogen recognition by phagocytic cells. In this study we observed that a fraction of S. aureus culture supernatant prevented binding of C3b to neutrophils. This fraction consisted of S. aureus leukocidins and Efb. The C-terminus of Efb is known to bind C3b and shares significant sequence homology to the extracellular complement binding protein [Ecb). Here we show that S. aureus Ecb displays various mechanisms to block bacterial recognition by neutrophils. The presence of Ecb blocked direct interaction between soluble CR1 and C3b and reduced the cofactor activity of CR1 in proteolytic inactivation of C3b. Furthermore, Ecb could dose-dependently prevent recognition of C3b by cell-bound CR1 that lead to impaired phagocytosis of NHS-opsonized S. aureus. Phagocytosis was furthermore reduced in the presence of soluble CR1 [sCR1). These data indicate that the staphylococcal protein Ecb prevents recognition of C3b opsonized bacteria by neutrophil CR1 leading to impaired killing by phagocytosis and thereby contribute to immune evasion 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.