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Staphylococcus aureus infection of human endothelial cells potentiates Fc receptor expression
V Bengualid1, V B Hatcher, B Diamond
1Department of Medicine, Montefiore Medical Center, Bronx, NY 10467.
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.
Insights
Staphylococcus aureus infection triggers Fc receptor expression on endothelial cells, potentially causing vasculitis. This Fc receptor involvement was confirmed through specific binding assays with antibody-coated red blood cells.
Area of Science:
- Immunology
- Microbiology
- Pathology
Background:
- Vasculitis is a known complication of staphylococcal-endovascular infections.
- Endothelial cell Fc receptors (FcR) may play a role in this complication.
- Staphylococcus aureus is a common pathogen in endovascular infections.
Purpose of the Study:
- To investigate the expression of FcR on endothelial cells infected with Staphylococcus aureus.
- To determine the mechanism and conditions for FcR expression during S. aureus infection.
- To elucidate the role of FcR in the pathogenesis of S. aureus-associated vasculitis.
Main Methods:
- Measurement of FcR on endothelial cells using chromium-51 labeled sheep red blood cells (SRBC) pre-incubated with rabbit anti-SRBC IgG.
- Testing binding with IgG and IgM labeled SRBC, and assessing the effect of aggregated IgG and F(ab')2 fragments.
- Correlation of FcR expression with bacterial density and phagocytosis.
Main Results:
- FcR were not detected on uninfected endothelial cells.
- FcR were demonstrated on S. aureus infected cells, specifically binding IgG-labeled SRBC.
- FcR expression required high bacterial density (≥ 8 x 10^7 cfu/ml) and staphylococcal phagocytosis, independent of new protein synthesis.
- Binding was specific to FcR, as indicated by blocking studies with aggregated IgG and lack of binding with F(ab')2 fragments.
Conclusions:
- Staphylococcus aureus invasion induces FcR expression on human endothelial cells.
- FcR expression on infected endothelial cells may contribute to the vasculitis seen in staphylococcal-endovascular infections.
- This finding provides a potential mechanism for immune-mediated damage in S. aureus infections.