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Complement activation influences Staphylococcus aureus adherence to endothelial cells.

K M Cunnion1, M M Frank

  • 1Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA. Cunniok@chkd.org

Infection and Immunity
|February 22, 2003
PubMed
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Staphylococcus aureus binding to endothelial cells is crucial for infection spread. Complement activation on bacteria reduces binding, while complement-activated cells increase it, impacting metastatic infection development.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Staphylococcus aureus adherence to endothelial cells (EC) is a key step in metastatic infection.
  • The role of the complement system in this adherence process was previously uninvestigated.

Purpose of the Study:

  • To investigate the role of complement in Staphylococcus aureus binding to endothelial cells.
  • To explore how complement activation on bacteria or endothelial cells affects adherence.

Main Methods:

  • Log-phase Staphylococcus aureus with minimal capsule expression was incubated with human serum under various conditions.
  • Bacteria were then incubated with cultured human umbilical vein endothelial cells.
  • Adherence was quantified visually after staining.

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Main Results:

  • Incubation in heat-inactivated serum increased S. aureus adherence by 488% compared to buffer.
  • Complement-active normal human serum (NHS) decreased bacterial binding to EC by 58% compared to heat-inactivated serum.
  • Complement activation on bacteria reduced adherence, while complement activation on EC increased S. aureus binding.

Conclusions:

  • Complement activation on the bacterial surface inhibits Staphylococcus aureus adherence to endothelial cells, partly via reduced binding to fibronectin.
  • Complement-activated endothelial cells exhibit increased Staphylococcus aureus binding, suggesting a dual role for complement in infection dynamics.
  • Bacterial capsule expression significantly interferes with S. aureus adherence to endothelial cells.