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Effects of staphylococcal toxic shock syndrome toxin 1 on aortic endothelial cells
Journal article   Peer reviewed

Effects of staphylococcal toxic shock syndrome toxin 1 on aortic endothelial cells

Peter K Lee, Gregory M Vercellotti, James R Deringer and Patrick M Schlievert
The Journal of infectious diseases, Vol.164(4), pp.711-719
10/1991
DOI: 10.1093/infdis/164.4.711
PMID: 1654356

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Abstract

In staphylococcal toxic shock syndrome, hypotension and shock due to capillary leak may rapidly lead to death of the host. To investigate its pathogenesis, the cytotoxic effects of toxic shock syndrome toxin 1 (TSST-1) on porcine aortic endothelial cells (PAEC) were examined in vitro. TSST-1 killed PAEC (as measured by 51Cr release) in a dose- and time-dependent fashion and was blocked by anti-TSST-1 antibodies. Receptor-mediated endocytosis may be critical for the cytotoxic effects of TSST-1, as killing was inhibited by cold (4 degrees C) and by addition of chloroquine and methylamine. Furthermore, calcium and oxygen appeared necessary for TSST-1 effects on PAEC. Membrane receptor binding studies indicated PAEC bind TSST-1 with high affinity (Kd = 5.7 x 10(-7) M) and had 2.2 x 10(4) receptors/cell. Last, as measured by 125I-labeled albumin flux in a transendothelial permeability model, TSST-1 enhanced the permeability of PAEC monolayers in a dose- and time-dependent manner.
Endothelium, Vascular - cytology Oxygen - pharmacology Temperature Enterotoxins - toxicity Humans Receptors, Cell Surface - analysis Cell Membrane Permeability Chloroquine - pharmacology Bacterial Toxins Swine Receptors, Peptide Methylamines - pharmacology Staphylococcus aureus Binding, Competitive Calcium - pharmacology Cells, Cultured Receptors, Enterotoxin Receptors, Guanylate Cyclase-Coupled Animals Guanylate Cyclase Endothelium, Vascular - metabolism Superantigens Enterotoxins - metabolism Aorta - cytology Kinetics Endotoxins - toxicity

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