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Cholera toxin mechanism. Cholera toxin (also known as choleragen and sometimes abbreviated to CTX, Ctx or CT) is an AB5 multimeric protein complex secreted by the bacterium Vibrio cholerae. [1] [2] CTX is responsible for the massive, watery diarrhea characteristic of cholera infection. [3] It is a member of the heat-labile enterotoxin family.
One chromosomes produces the cholera toxin (CT), a protein that causes profuse, watery diarrhea (known as "rice-water stool"). [5] But the DNA does not directly code for the toxin as the genes for cholera toxin are carried by CTXphi (CTXφ), a temperate bacteriophage (virus). The virus only produces the toxin when inserted into the bacterial DNA.
This toxin has the ability to disrupt electrolyte balance in intestinal epithelial cells which can lead to issues including severe diarrhea, which is known to be a common symptom of this toxin. [15] In addition to the cholera toxin, there are other virulence factors such as surface adhesins, which are essential in helping the bacteria to adhere ...
After their B subunit binds to receptors on the cell surface, the toxin is enveloped by the cell and transported inside either through clathrin-dependent endocytosis or clathrin-independent endocytosis. [21] The mechanism pathways for the four AB5 toxins: cholera toxin, pertussis toxin, shiga toxin, and subtilase cytotoxin.
CTXφ is generally present and integrated into the genome of the V. cholerae bacterium, and more rarely in a virion from outside the bacterium. While integrated into the bacterial genome, CTX prophages are found on each of the two chromosomes (in the O1 serogroup of V. cholerae) or arranged in tandem on the larger chromosome (in the El Tor biotype of V. cholerae). [2]
V. cholerae is the most common pathogen that causes cholera. The gold standard for detecting cholera is through cultures of stool samples or rectal swabs. Identification is then done through microscopy or by agglutination of antibodies. [25] Cultures are done in thiosulfate citrate bile-salts sucrose agar. V cholerae will form yellow colonies. [26]
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.
Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact with host cell mechanisms to pump chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The chloride and sodium ions create a salt-water ...