Journal article
Effects of staphylococcal toxic shock syndrome toxin 1 on aortic endothelial cells
The Journal of infectious diseases, Vol.164(4), pp.711-719
10/1991
DOI: 10.1093/infdis/164.4.711
PMID: 1654356
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.
Details
- Title: Subtitle
- Effects of staphylococcal toxic shock syndrome toxin 1 on aortic endothelial cells
- Creators
- Peter K Lee - Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455-0312Gregory M VercellottiJames R DeringerPatrick M Schlievert
- Resource Type
- Journal article
- Publication Details
- The Journal of infectious diseases, Vol.164(4), pp.711-719
- DOI
- 10.1093/infdis/164.4.711
- PMID
- 1654356
- NLM abbreviation
- J Infect Dis
- ISSN
- 0022-1899
- eISSN
- 1537-6613
- Publisher
- United States
- Grant note
- CA-0913 / NCI NIH HHS HL-36611 / NHLBI NIH HHS HL-33793 / NHLBI NIH HHS
- Language
- English
- Date published
- 10/1991
- Academic Unit
- Microbiology and Immunology; Internal Medicine
- Record Identifier
- 9984001110202771
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