Cholera toxin

Robert Koch, a German physician and microbiologist, was the first person to postulate the existence of cholera toxin.

[4] Koch's postulation was proven correct by Indian microbiologist Sambhu Nath De, who in 1951 studied and documented the effects of injecting rabbits with heat-killed cholera bacteria.

[5] In 1959, De conducted another experiment, this time using a bacteria-free culture filtrate from V. cholerae injected into the small intestines of rabbits.

[9] This structure is similar in shape, mechanism, and sequence to the heat-labile enterotoxin secreted by some strains of the Escherichia coli bacterium.

The combined effects result in rapid fluid loss from the intestine, up to 2 liters per hour, leading to severe dehydration and other factors associated with cholera, including a rice-water stool.

[17] Because the B subunit appears to be relatively non-toxic, researchers have found a number of applications for it in cell and molecular biology.

[18] Treatment of cultured rodent neural stem cells with cholera toxin induces changes in the localization of the transcription factor Hes3 and increases their numbers.

B subunit complexes labelled with fluorescent tags or subsequently targeted with antibodies can be used to identify rafts.

Some studies suggest that the inclusion of rCTB may improve vaccine efficacy in young children (2-10) and increase the duration of protection.

[20] Since cholera toxin has been shown to preferentially bind to GM1 gangliosides, this characteristic can be utilized for membrane studies.

Lipid rafts are difficult to study as they vary in size and lifetime, as well being part of an extremely dynamic component of cells.

[21] Endocytosis is broadly divided into clathrin-dependent and clathrin-independent process, and the cholera toxin utilizes both pathways.