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Quantifying the Cytotoxicity of Staphylococcus aureus Against Human Polymorphonuclear Leukocytes
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Complement regulator C4BP binds to Staphylococcus aureus and decreases opsonization.

Pamela S Hair1, Sara M Wagner, Patricia T Friederich

  • 1Department of Pediatrics, Eastern Virginia Medical School, Norfolk, VA 23501-1980, USA.

Molecular Immunology
|February 16, 2012
PubMed
Summary
This summary is machine-generated.

Staphylococcus aureus evades immune detection by binding C4b-binding protein (C4BP). This protein inhibits complement system components, aiding bacterial survival in infections.

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Area of Science:

  • Immunology
  • Microbiology
  • Biochemistry

Background:

  • Staphylococcus aureus is a significant pathogen causing diverse infections.
  • The complement system is crucial for controlling bacterial infections.
  • Complement regulatory proteins, such as C4b-binding protein (C4BP), can be exploited by pathogens to evade immune responses.

Purpose of the Study:

  • To investigate the interaction between Staphylococcus aureus and C4b-binding protein (C4BP).
  • To elucidate the role of C4BP in the immune evasion strategies of S. aureus.

Main Methods:

  • Experiments involving S. aureus opsonization with C4b in serum.
  • Assessment of C4BP binding to S. aureus.
  • Analysis of C4BP's cofactor activity for factor I-mediated C4b cleavage.
  • Evaluation of C4BP's effect on complement component deposition on the bacterial surface.

Main Results:

  • S. aureus rapidly binds C4b in serum, primarily initiated by anti-staphylococcal antibodies.
  • Bound C4b is quickly inactivated to iC4b and C4d.
  • Clinical S. aureus strains efficiently bind C4BP from serum and purified C4BP.
  • C4BP on the S. aureus surface acts as a cofactor for factor I, cleaving C4b.
  • C4BP inhibits classical pathway C3-convertase activity, reducing C3b deposition.

Conclusions:

  • C4BP is recruited to the S. aureus surface.
  • C4BP inhibits C4 complement effectors on S. aureus.
  • This interaction represents a novel immune evasion mechanism for Staphylococcus aureus.