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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.
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.
The binding site is between beta sheets eight and nine. This allows the human claudin-3,4,6,7,8 and 14 to bind but not 1,2,5, and 10. The way the protein work is it destroys the cell membrane structure of animals by binding to claudin family proteins. These are components of tight junctions of the epithelial cell membrane.
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. [citation needed]
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.
Atlantic horseshoe crab Limulus polyphemus. Limulus amebocyte lysate (LAL) is an aqueous extract of motile blood cells from the Atlantic horseshoe crab Limulus polyphemus.LAL reacts with bacterial endotoxins such as lipopolysaccharides (LPS), which are components of the bacterial capsule, the outermost membrane of cell envelope of gram-negative bacteria.
Studies have shown that esophageal cancer can be related back to corn grain that contains fumonisins. [38] Other effects from fumonisins are birth defects of the brain, spine, and spinal cord. [38] In animals, problems with the pulmonary edema and hydrothorax swines have been proven to have association with fumonisins. [38]
Domain A1 (approximately 22kDa in cholera toxin or heat labile enterotoxins) is the part of the toxin responsible for its toxic effects. Domain A2 (approximately 5kDa in cholera toxin or heat labile enterotoxin) provides a non-covalent linkage to the B subunit through the B subunit's central pore. [ 5 ]