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Toxins 2010, 2(12), 2769-2794; doi:10.3390/toxins2122769

Escherichia coli Shiga Toxin Mechanisms of Action in Renal Disease

Department of Microbiology and Immunology, School of Medicine, University of Maryland, 685 W. Baltimore St., HSF I Suite 380, Baltimore, MD 21201, USA
Received: 20 October 2010 / Revised: 13 November 2010 / Accepted: 24 November 2010 / Published: 2 December 2010
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Abstract

Shiga toxin-producing Escherichia coli is a contaminant of food and water that in humans causes a diarrheal prodrome followed by more severe disease of the kidneys and an array of symptoms of the central nervous system. The systemic disease is a complex referred to as diarrhea-associated hemolytic uremic syndrome (D+HUS). D+HUS is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure. This review focuses on the renal aspects of D+HUS. Current knowledge of this renal disease is derived from a combination of human samples, animal models of D+HUS, and interaction of Shiga toxin with isolated renal cell types. Shiga toxin is a multi-subunit protein complex that binds to a glycosphingolipid receptor, Gb3, on select eukaryotic cell types. Location of Gb3 in the kidney is predictive of the sites of action of Shiga toxin. However, the toxin is cytotoxic to some, but not all cell types that express Gb3. It also can cause apoptosis or generate an inflammatory response in some cells. Together, this myriad of results is responsible for D+HUS disease.
Keywords: Shiga toxin; kidney; HUS; Gb3; animal model; renal failure; E. coli Shiga toxin; kidney; HUS; Gb3; animal model; renal failure; E. coli
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Obrig, T.G. Escherichia coli Shiga Toxin Mechanisms of Action in Renal Disease. Toxins 2010, 2, 2769-2794.

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