The endotoxin content, determined using a kinetic chromogenic LAL assay, is <90 EU/mg.
Alternative Names
Stx2
Purity
>95%
Format
Liquid
Buffer
10 mM PBS
Preservative
None
Storage
Store at -20°C
Citations
Publication ()
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Background
Escherichia coli (E. coli) Shiga toxin, also known as Shiga toxin-producing E. coli (STEC) toxin or verotoxin, is a virulence factor produced by certain strains of E. coli bacteria. Shiga toxins are classified into two main types: Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2). These toxins are named after the Japanese bacteriologist Kiyoshi Shiga, who first described them.
Stx are composed of two subunits, A and B. The B subunit is responsible for recognizing and binding to specific receptors on the surface of target cells. The A subunit possesses enzymatic activity and exerts cytotoxic effects on cells. Stx are notorious for their ability to inhibit protein synthesis in host cells, leading to cell death and tissue damage. One of the key receptors recognized by Stx is globotriaosylceramide (Gb3), which is expressed on the surface of certain cells, particularly in the kidneys and the endothelial lining of blood vessels. The binding of Stx to Gb3-expressing cells triggers a cascade of events that can lead to a range of clinical manifestations, from mild gastrointestinal symptoms such as diarrhea and abdominal cramps to more severe forms such as hemorrhagic colitis and hemolytic uremic syndrome (HUS). HUS is a potentially life-threatening condition characterized by the destruction of red blood cells, low platelet count, and kidney damage, particularly in young children and the elderly.
Figure 1. STEC infection may develop into potentially fatal complications, such as HUS. (Source: Kim, J. S. et al., 2020)
STEC strains, which produce Shiga toxins, are a major cause of foodborne illnesses and outbreaks worldwide. Contaminated food and water, especially undercooked ground beef, unpasteurized milk, and dairy products, contaminated vegetables and fruits, and contaminated water sources, are common routes of transmission. Person-to-person transmission can also occur, particularly in settings with inadequate hygiene practices. Prevention and control of STEC infections involve implementing good food safety practices, such as proper cooking and handling of food, pasteurization of milk, and practicing good personal hygiene, including handwashing. Prompt identification of outbreaks and appropriate public health interventions are crucial in minimizing the spread of these infections and providing timely medical care for affected individuals.
1. Kim J S, et al. Recent updates on outbreaks of Shiga toxin-producing Escherichia coli and its potential reservoirs. Frontiers in Cellular and Infection Microbiology. 2020, 10: 273.
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References
Crosstalk between Human Microvascular Endothelial Cells and Tubular Epithelial Cells Modulates Pro-Inflammatory Responses Induced by Shiga Toxin Type 2 and Subtilase Cytotoxin
TOXINS
Authors: Alvarez, Romina S.; Jancic, Carolina; Garimano, Nicolas; Sacerdoti, Flavia; Paton, Adrienne W.; Paton, James C.; Ibarra, Cristina; Amaral, Maria M.
Hemolytic uremic syndrome (HUS) is a consequence of Shiga toxin (Stx)-producing Escherichia coli (STEC) infection and is the most frequent cause of acute renal failure (ARF) in children. Subtilase cytotoxin (SubAB) has also been associated with HUS pathogenesis. We previously reported that Stx2 and SubAB cause different effects on co-cultures of human renal microvascular endothelial cells (HGEC) and human proximal tubular epithelial cells (HK-2) relative to HGEC and HK-2 monocultures. In this work we have analyzed the secretion of pro-inflammatory cytokines by co-cultures compared to monocultures exposed or not to Stx2, SubAB, and Stx2+SubAB. Under basal conditions, IL-6, IL-8 and TNF-alpha secretion was different between monocultures and co-cultures. After toxin treatments, high concentrations of Stx2 and SubAB decreased cytokine secretion by HGEC monocultures, but in contrast, low toxin concentrations increased their release. Toxins did not modulate the cytokine secretion by HK-2 monocultures, but increased their release in the HK-2 co-culture compartment. In addition, HK-2 monocultures were stimulated to release IL-8 after incubation with HGEC conditioned media. Finally, Stx2 and SubAB were detected in HGEC and HK-2 cells from the co-cultures. This work describes, for the first time, the inflammatory responses induced by Stx2 and SubAB, in a crosstalk model of renal endothelial and epithelial cells.
Shiga toxins—from cell biology to biomedical applications
Shiga toxin-producing Escherichia coli is an emergent pathogen that can induce haemolytic uraemic syndrome. The toxin has received considerable attention not only from microbiologists but also in the field of cell biology, where it has become a powerful tool to study intracellular trafficking. In this Review, we summarize the Shiga toxin family members and their structures, receptors, trafficking pathways and cellular targets. We discuss how Shiga toxin affects cells not only by inhibiting protein biosynthesis but also through the induction of signalling cascades that lead to apoptosis. Finally, we discuss how Shiga toxins might be exploited in cancer therapy and immunotherapy.
Pathogenesis of Shiga-Toxin Producing Escherichia coli
Ricin and Shiga Toxins: Pathogenesis, Immunity, Vaccines and Therapeutics
Shiga toxin (Stx)-producing Escherichia coli (STEC) are food-borne pathogens that cause hemorrhagic colitis and a serious sequela, the hemolytic uremic syndrome (HUS). The largest outbreaks of STEC are due to a single E. coli serotype, O157:H7, although non-O157 serotypes also cause the same diseases. Two immunologically distinct Stxs are found in E. coli, Stx1 and Stx2. The Stxs are AB5 toxins that halt protein synthesis in the host cell, a process that may lead to an apoptotic cell death. Stx-mediated damage to renal glomerular endothelial cells is hypothesized as the precipitating event for HUS. A subset of STEC referred to as the enterohemorrhagic E. coli has the capacity to intimately attach to and efface intestinal epithelial cells, a pathology called the A/E lesion. The A/E lesion is mediated by the adhesin intimin, its bacterially encoded receptor, Tir, and effectors secreted through a type III secretion system. The proteins needed for the A/E lesion are encoded within a large pathogenicity island called the locus of enterocyte effacement or LEE. There are several animal models for STEC infection, but no one model fully represents the spectrum of STEC illness. Currently there is no cure for STEC infection, and therapies are based mainly on alleviating symptoms. However, chimeric or humanized monoclonal antibodies have been developed that neutralize the Stxs, and those therapies may be able to prevent the development of HUS in an STEC-infected patient.
COA
Publication 
Figure 1. STEC infection may develop into potentially fatal complications, such as HUS.![The purity of recombinant shiga toxin 2 subunit b [His] >98%, determined by SDS-PAGE](https://resource.creative-diagnostics.com/diagnostics/productimages-1/DAGA-878-1.jpg)
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