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Visualization of Bacterial Toxin Induced Responses Using Live Cell Fluorescence Microscopy
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Clostridium perfringens beta-toxin forms multimeric transmembrane pores in human endothelial cells

V Steinthorsdottir1, H Halldórsson, O S Andrésson

  • 1Institute for Experimental Pathology, University of Iceland, Reykjavik, Keldur, 112, Iceland. vstein@decode.is

Microbial Pathogenesis
|January 7, 2000
PubMed

Insights

Clostridium perfringens beta-toxin, like Staphylococcus aureus alpha-toxin, forms pores in human endothelial cells. This pore formation causes cell damage, with effects correlating to toxin lethality in mice.

Area of Science:

  • Microbiology
  • Toxicology
  • Cell Biology

Background:

  • Beta-toxin is a lethal toxin produced by Clostridium perfringens.
  • Sequence and structural studies suggest homology between beta-toxin and Staphylococcus aureus alpha-toxin.
  • Human endothelial cells are known targets of alpha-toxin.

Purpose of the Study:

  • To investigate the functional effects of beta-toxin on human umbilical vein endothelial cells.
  • To compare the cellular mechanisms of beta-toxin and alpha-toxin.
  • To determine the cell specificity and pore-forming capabilities of beta-toxin.

Main Methods:

  • Exposure of human umbilical vein endothelial cells to beta-toxin and alpha-toxin.
  • Measurement of arachidonic acid and inositol release.
  • Analysis of toxin mutant effects and multimer formation in cell membranes.
  • Correlation of in vitro effects with in vivo mouse lethality data.

Main Results:

  • Beta-toxin induced dose-dependent release of arachidonic acid from endothelial cells, similar to alpha-toxin.
  • Both toxins caused inositol leakage, indicating transmembrane pore formation.
  • Mutant toxin effects on cells correlated with their lethal doses in mice.
  • Heat-stable beta-toxin multimers formed specifically in the membranes of tested endothelial cells.

Conclusions:

  • Beta-toxin functions as a cell-specific pore-forming toxin.
  • Beta-toxin is structurally and functionally related to Staphylococcus aureus alpha-toxin.
  • Endothelial cell membrane interactions and multimerization are key features of beta-toxin activity.

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