Membrane cholesterol is required for activity of Vibrio vulnificus cytolysin

Arch Microbiol. 2007 Jun;187(6):467-73. doi: 10.1007/s00203-007-0214-0. Epub 2007 Feb 7.

Abstract

Vibrio vulnificus cytolysin (VVC) forms a pore in the plasma membrane and induces cytolysis of various cells including erythrocytes, neutrophil and endothelial cells. The cytolytic activity of VVC is inhibited by exogenously added cholesterol, suggesting that membrane cholesterol might be required for VVC cytolytic activity. However, there is no direct evidence that membrane cholesterol is involved in VVC-induced cytolysis. Herein we demonstrate that membrane cholesterol is required for binding of VVC to the plasma membrane. Membrane cholesterol depletion with methyl-beta-cyclodextrin inhibited VVC-induced K(+) release, 2-deoxy glucose release and Ca(2+) influx, which are indicators of VVC pore formation. The cholesterol depletion-induced blockage of VVC cytolysis was due to the inhibition of VVC binding to membrane. These findings suggest that interaction with cholesterol is required for activity of VVC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Membrane / chemistry*
  • Cell Membrane / metabolism
  • Cholesterol / metabolism*
  • Erythrocytes / physiology
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Neutrophils / microbiology
  • Perforin
  • Pore Forming Cytotoxic Proteins / metabolism*
  • Rats
  • Vibrio vulnificus / metabolism*
  • Vibrio vulnificus / pathogenicity*
  • beta-Cyclodextrins / pharmacology

Substances

  • Membrane Glycoproteins
  • Pore Forming Cytotoxic Proteins
  • beta-Cyclodextrins
  • methyl-beta-cyclodextrin
  • Perforin
  • Cholesterol