Staphylococcus aureus infection of human endothelial cells potentiates Fc receptor expression

J Immunol. 1990 Dec 15;145(12):4279-83.

Abstract

Vasculitis, a recognized complication of staphylococcal-endovascular infections, may result in part, from the expression of FcR by Staphylococcus aureus-infected endothelial cells. FcR were measured using [51]Cr labeled SRBC preincubated with rabbit anti-SRBC IgG. FcR were not detected on uninfected endothelial cells, but were demonstrated on S. aureus infected cells using IgG, but not IgM labeled SRBC. FcR expression was dependent on the initial bacterial density (greater than or equal to 8 x 10(7) cfu/ml) and on phagocytosis of the staphylococci, but not on new protein synthesis. IgG labeled SRBC binding was blocked by aggregated IgG but not IgM. SRBC coated with the F(ab')2 portion of IgG did not bind, thus confirming that FcR were specifically involved in this interaction. FcR are expressed after S. aureus invasion of human endothelial cells and may contribute to the vasculitis which often accompanies S. aureus-endovascular infections.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cells, Cultured
  • Cycloheximide / pharmacology
  • Endothelium, Vascular / immunology*
  • Endothelium, Vascular / microbiology
  • Humans
  • In Vitro Techniques
  • Receptors, Fc / metabolism*
  • Species Specificity
  • Staphylococcal Infections / immunology*
  • Staphylococcal Protein A / analysis
  • Staphylococcus aureus / classification
  • Time Factors

Substances

  • Receptors, Fc
  • Staphylococcal Protein A
  • Cycloheximide