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Enterotoxins have a particularly marked effect upon the gastrointestinal tract, causing traveler's diarrhea and food poisoning. The action of enterotoxins leads to increased chloride ion permeability of the apical membrane of intestinal mucosal cells.
In addition to its effects on chloride secretion, which involve the same steps as the effects of cholera toxin, Elt binds additional substrates: lipopolysaccharide on the surface of E. coli cells and A-type blood antigens. [2] The importance of these binding events is not yet known.
Different STs recognize distinct receptors on the surface of animal cells and thereby affect different intracellular signaling pathways. For example, STa enterotoxins bind and activate membrane-bound guanylate cyclase, which leads to the intracellular accumulation of cyclic GMP and downstream effects on several signaling pathways.
In the field of molecular biology, enterotoxin type B, also known as Staphylococcal enterotoxin B (SEB), is an enterotoxin produced by the gram-positive bacteria Staphylococcus aureus.
Enterotoxigenic Escherichia coli (ETEC) is a type of Escherichia coli and one of the leading bacterial causes of diarrhea in the developing world, [1] as well as the most common cause of travelers' diarrhea. [2]
Enterotoxins are chromosomally encoded exotoxins that are produced and secreted from several bacterial organisms. It is a heat stable toxin and is resistant to digestive protease . [ 5 ] [ 6 ] It is the ingestion of the toxin that causes the inflammation and swelling of the intestine.
Clostridium enterotoxins are toxins produced by Clostridium species. [2] Clostridial species are one of the major causes of food poisoning / gastrointestinal illnesses . They are anaerobic , [ 1 ] gram-positive, spore-forming rods that occur naturally in the soil. [ 3 ]
The rotavirus nonstructural protein NSP4 was the first viral enterotoxin discovered. [1] It is a viroporin [2] and induces diarrhea and causes Ca 2+-dependent transepithelial secretion.