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Inhibition of Complement Activation by a SecretedStaphylococcus aureusProtein
- Source :
- The Journal of Infectious Diseases. 190:571-579
- Publication Year :
- 2004
- Publisher :
- Oxford University Press (OUP), 2004.
-
Abstract
- Staphylococcus aureus can cause a variety of acute and chronic diseases. The ability of S. aureus to cause persistent infections has been linked to its ability to evade or inactivate host immune responses. We have identified a secreted 19-kDa protein produced by S. aureus that binds to the complement protein C3. N-terminal sequencing of this protein identified it as the extracellular fibrinogen-binding protein (Efb). In this study, we demonstrate that Efb can bind to the alpha -chain of C3 and inhibit both the classical and alternative pathways of complement activation. In addition, we show that Efb can inhibit complement-mediated opsonophagocytosis in a dose-dependent manner and that Efb inhibits complement activity by blocking deposition of C3 or by preventing further complement activation beyond C3b. These data suggest that Efb is a virulence factor involved in facilitating persistent S. aureus infections by interfering with complement activity in vivo.
- Subjects :
- Staphylococcus aureus
Virulence Factors
Complement Pathway, Alternative
HL-60 Cells
medicine.disease_cause
Virulence factor
Microbiology
Immune system
Bacterial Proteins
Phagocytosis
Extracellular
medicine
Humans
Immunology and Allergy
Secretion
Complement Pathway, Classical
Complement Activation
biology
Complement C3
Opsonin Proteins
Recombinant Proteins
Complement system
Infectious Diseases
Factor H
biology.protein
Antibody
Carrier Proteins
Subjects
Details
- ISSN :
- 15376613 and 00221899
- Volume :
- 190
- Database :
- OpenAIRE
- Journal :
- The Journal of Infectious Diseases
- Accession number :
- edsair.doi.dedup.....fb73b580be514d8380b6b25e2129a7af