EntA; Enterotoxin type A; Staphylococcus enterotoxin A; Staphylococcus enterotoxin type A
Purity
> 95% as determined by SDS-PAGE
Format
Liquid
Concentration
Batch dependent - please inquire should you have specific requirements
Buffer
0.01 M PBS, pH7.3
Preservative
None
Storage
Store at -20°C to -80°C
Introduction
The S. aureus enterotoxins (SEs) are potent gastrointestinal exotoxins synthesized by S. aureus throughout the logarithmic phase of growth or during the transition from the exponential to the stationary phase. They are active in high nanogram to low microgram quantities, and are resistant to conditions (heat treatment, low pH) that easily destroy the bacteria that produce them, and to proteolytic enzymes, hence retaining their activity in the digestive tract after ingestion.
Keywords
Staphylococcus aureus; Enterotoxins; SEs
Citations
Publication ()
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Background
Staphylococcal enterotoxins are members of a family of more than 20 different staphylococcal and streptococcal exotoxins. These toxins are closely related and share similar sequences. They are known to cause the intoxication staphylococcal food poisoning syndrome, which is characterized by high fever, hypotension, diarrhea, shock, and in some cases death. There are five major SE toxins: SEA, SEB, SEC, SED, and SEE. The amino acid sequences of staphylococcal enterotoxins have been analyzed and found to consist of single-chain polypeptides. These polypeptides contain a unique cysteine loop formed by a disulfide bond between two half cystines located in the middle of the chain. Among these toxins, staphylococcus aureus Enterotoxin A (SEA) is the most frequently encountered toxin in cases of staphylococcal food poisoning.
SEA is a single-chain protein consisting of 233 amino acids with a molecular weight of 27,078 Da. It acts as a superantigen and is associated with various syndromes in animals (such as mastitis) and humans (including emesis, diarrhea, atopic dermatitis, arthritis, and toxic shock). SEA exerts its effects by binding to specific regions on major histocompatibility complex (MHC) class II molecules found on antigen-presenting cells (APCs) and to the variable region (Vss) on T-cell receptors. By forming a bridge between T cells and APCs, the toxin triggers the proliferation of a significant proportion of T cells (around 20%). This excessive T-cell activation leads to the release of cytokines, signaling molecules that play a role in immune responses. This activation of the immune system can result in a cascade of inflammatory responses, contributing to the clinical manifestations of staphylococcal infections.
Alternative Names
Recombinant Staphylococcus aureus EntA Recombinant Staphylococcus aureus Enterotoxin type A Recombinant S. aureus Enterotoxin A (SEA) Recombinant S. aureus EntA Recombinant S. aureus Enterotoxin type A
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References
Food Poisoning and Staphylococcus aureus Enterotoxins
Staphylococcus aureus produces a wide variety of toxins including staphylococcal enterotoxins (SEs; SEA to SEE, SEG to SEI, SER to SET) with demonstrated emetic activity, and staphylococcal-like (SEl) proteins, which are not emetic in a primate model (SElL and SElQ) or have yet to be tested (SElJ, SElK, SElM to SElP, SElU, SElU2 and SElV). SEs and SEls have been traditionally subdivided into classical (SEA to SEE) and new (SEG to SElU2) types. All possess superantigenic activity and are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, vSa genomic islands, or by genes located next to the staphylococcal cassette chromosome (SCC) implicated in methicillin resistance. SEs are a major cause of food poisoning, which typically occurs after ingestion of different foods, particularly processed meat and dairy products, contaminated with S. aureus by improper handling and subsequent storage at elevated temperatures. Symptoms are of rapid onset and include nausea and violent vomiting, with or without diarrhea. The illness is usually self-limiting and only occasionally it is severe enough to warrant hospitalization. SEA is the most common cause of staphylococcal food poisoning worldwide, but the involvement of other classical SEs has been also demonstrated. Of the new SE/SEls, only SEH have clearly been associated with food poisoning. However, genes encoding novel SEs as well as SEls with untested emetic activity are widely represented in S. aureus, and their role in pathogenesis may be underestimated.
Staphylococcus aureus Growth and Enterotoxin A Production in an Anaerobic Environment
The effects of strict anaerobic conditions on the growth of Staphylococcus aureus and the production of staphylococcal enterotoxin A (SEA) were studied. The growth of S. aureus, a facultative anaerobic bacterium, is slower anaerobically than aerobically. When grown on brain heart infusion broth at 37°C, the anaerobic generation time at mid-log phase was 80 min, compared with 35 min for the aerobic control. In contrast to previous studies demonstrating that staphylococcal cell density was 9- to 17-fold greater in aerobic than in anaerobic cultures, data for a staphylococcal strain implicated in food poisoning showed that the cell density was only two to three times as great in aerobic cultures. Production of SEA was monitored by Western immunoblotting and shown to be growth dependent. With slower anaerobic growth, relatively less toxin was produced than under aerobic conditions, but in both cases SEA was detected after 120 min of incubation. The combined effects of temperature and aeration on S. aureus were also studied. Growth and toxin production of aerobic and anaerobic cultures at temperatures ranging from 14 to 37°C were analyzed. Growth was still observed at low temperatures in both environments. A linear model for S. aureus aerobic or anaerobic growth as a function of incubation temperature was developed from these studies. The model was tested from 17 to 35.5°C, and the results suggest that the model can accurately predict the S. aureus growth rate in this temperature range. The data suggest that anaerobic conditions are not an effective barrier against S. aureus growth.