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.
Highlights
This review focuses on the kidney disease caused by Shiga toxin-producing E. coli, referred to as diarrhea-associated hemolytic uremic syndrome (D+HUS)
What this means for D+HUS kidney disease is that it remains important to determine where and how much Gb3 is localized to different renal cell types, and if the Gb3 is reactive with Stx1 or the host response to Shiga toxin (Stx) should represent a change in physiology consistent with the known function of the cell type
Results from the mouse model of D+HUS have been instructive for kidney disease whether beginning from oral Shiga Toxin-Producing E. coli (STEC) or injected (i.p. or i.v.) Stx1 and Shiga toxin type 2 (Stx2) [39,76,90,92,93,95,101,102,103,104]
Summary
This review focuses on the kidney disease caused by Shiga toxin-producing E. coli, referred to as diarrhea-associated hemolytic uremic syndrome (D+HUS). The animal models discussed are referred to a D+HUS models, some of these do not include a diarrheal phase They all result in renal disease related to Shiga toxin action and exhibit aspects of D+HUS in humans. It is here that a stool sample is taken for analysis of STEC and Shiga toxin It is during the hemorrhagic colitis stage that Stx and/or Stx enter the blood circulation setting in action a series of toxemic reactions that culminate in renal failure in 5–15% of the patients. The most common form of STEC is E. coli O157:H7, there are other E. coli serotypes that produce Stx and/or Stx which cause D+HUS [31,32]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
