Inhibition of complement activation by a secreted Staphylococcus aureus protein

Lawrence Y.L. Lee, Magnus Hook, David Haviland, Rick A. Wetsel, Edward O. Yonter, Peter Syribeys, John Vernachio, Eric L. Brown

Research output: Contribution to journalArticle

98 Scopus citations

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 α-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.

Original languageEnglish (US)
Pages (from-to)571-579
Number of pages9
JournalJournal of Infectious Diseases
Volume190
Issue number3
DOIs
StatePublished - Aug 1 2004

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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