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An enterotoxin is a protein exotoxin released by a microorganism that targets the intestines. [1] They can be chromosomally or plasmid encoded. [ 2 ] They are heat labile (> 60 °C), of low molecular weight and water-soluble.
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 toxic activity of LPS was first discovered and termed endotoxin by Richard Friedrich Johannes Pfeiffer.He distinguished between exotoxins, toxins that are released by bacteria into the surrounding environment, and endotoxins, which are toxins "within" the bacterial cell and released only after destruction of the bacterial outer membrane. [11]
An exotoxin is a toxin secreted by bacteria. [1] An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host. Exotoxins may be secreted, or, similar to endotoxins, may be released during lysis of the cell.
Endotoxins most commonly refer to the lipopolysaccharide (LPS) or lipooligosaccharide (LOS) that are in the outer plasma membrane of Gram-negative bacteria. The botulinum toxin , which is primarily produced by Clostridium botulinum and less frequently by other Clostridium species, is the most toxic substance known in the world. [ 1 ]
Shiga toxin type 1 and type 2 (Stx-1 and 2) are the Shiga toxins produced by some E. coli strains. Stx-1 is identical to Stx of Shigella spp. or differs by only one amino acid. [6] Stx-2 shares 55% amino acid homology with Stx-1. [7] Cytotoxins – an archaic denotation for Stx – is used in a broad sense.
Endotoxin is a component (lipopolysaccharide (LPS)) of the cell wall of gram-negative bacteria. It is the lipid A part of this LPS which is toxic. [4] Lipid A is an endotoxin. Endotoxins trigger intense inflammation. They bind to receptors on monocytes causing the release of inflammatory mediators which induce degranulation. As part of this ...
Earlier research established TcdA strictly as an enterotoxin, and TcdB as a cytotoxin, but later both toxins were found to have the same mechanism of action. [6] To fully investigate the role of both toxins in pathogenesis of C. difficile infection, a gene knockout system in a hamster infection model was developed.