U.S. Department of Defense


Date of this Version



The Journal of Infectious Diseases (1991), 164: 344-52.


Infection with Shinga toxin- and Shinga-like toxin -producing strains of Shigella dysenteriae and Escherichia coli, respectively, can progress to the hemolytic-uremic syndrome. It has been hypothesized that circulating Shinga toxin, Shinga-like toxins, and endotoxins may contribute to the disease by directly damaging glomerular endothelial cells. The effects of these toxins on HeLa, Vero, and human vascular endothelial cells (EC) were examined. Confluent EC were sensitive to Shinga toxin but were at least 106-fold less sensitive to the toxins than were Vero cells. Shinga toxin was the predominant cytotoxic factor. Lipopolysaccharides were not cytotoxic and did not augment Shinga toxin-mediated toxicity. Lower doses of Shinga toxin caused cytooxicity when coincubated with tumor necrosis factor. The relative resistance of EC to Shinga toxin and Shinga-like toxins may be due to reduced toxin binding, as low levels of globotriaosylceramide (Gb3), the toxin-specific receptor, were found in EC membranes.