Specific Interaction of Escherichia coli O157:H7-Derived Shiga-like Toxin II with Human Renal Endothelial Cells

• Published in: The Journal of infectious diseases Vol. 172; no. 5; pp. 1397 - 1401
• Main Authors: Louise, Chandra B., Obrig, Tom G.
• Format: Journal Article
• Language: English
• Published: Chicago, IL University of Chicago Press 01-11-1995
• Subjects: Bacterial Toxins - metabolism; Bacterial Toxins - toxicity; Bacteriology; Biological and medical sciences; Cell Survival - drug effects; Cells, Cultured; Concise Communications; Cytotoxicity; Dose-Response Relationship, Drug; Endothelial cells; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - pathology; Enterotoxins - toxicity; Escherichia coli; Fundamental and applied biological sciences. Psychology; Glycolipids - metabolism; Hemolytic uremic syndrome; Human umbilical vein endothelial cells; Humans; Kinetics; Microbiology; Microcirculation; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Reagents; Receptors; Receptors, Cell Surface - metabolism; Renal Circulation; Shiga Toxin 1; Shiga Toxin 2; Shiga toxins; Toxins; Umbilical Cord; Viability; Human; Pathogenicity; Cell culture; Endothelial cell; Urinary system disease; Escherichia coli; Bacteria; Host agent relation; In vitro; Kidney; Enterobacteriaceae
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/172.5.1397

In Escherichia coli O157:H7 foodborne infections of humans, the Shiga-like toxins (SLTs) are thought to be the cause of life-threatening vascular complications, including acute renal disease known as hemolytic uremic syndrome or HUS. As virtually all E. coli O157:H7 isolates from HUS patients produce SLT-II (vs. SLT-I), the possible preferential interaction of SLT-II with human renal microvascular endothelial cells (HRMEC), the putative target of the SLTs in the development of HUS, was studied. SLT-II was 1000 times more potent a cytotoxic agent than SLT-I toward HRMEC. Toxin binding studies showed that this occurred although HRMEC could bind 10 times more SLT-I than SLT-II. This preferential action of SLT-II was specific for renal endothelial cells, as human umbilical vein endothelial cells were almost equally affected by SLT-I and SLT-II.