Cholera: current findings on pathophysiology The updated model of cholera extends beyond the enterocyte itself to include pines

(the neuroimmunoendocrine system-paracrine, immune, neurological, and endocrine system) and the intestinal smooth muscle. In addition to the classic cholera toxin (CT), two other toxins have been identified: zona occludens toxin (ZOT), which "loosens" the tight junctions, and accessory cholera toxin (ACE), the function of which is unknown. The intracellular processing of cholera toxin involves at least two discrete steps before reaching the basolateral adenylate cyclase; these steps are sensitive to either brefeldin A, an inhibitor of vesicular trafficking, or to temperature. Cholera toxin targets both enteric neurons and endocrine cells (EC), stimulating the release of

prostaglandins, serotonin, and vasoactive intestinal polypeptide, which amplify considerably the direct effects of the toxin on the enterocyte. Stimulation of the enteric nervous system by cholera toxin also significantly alters motor function. Thus, cholera toxin activates a full panoply of secretory stimuli that contribute to diarrhea. (GastroAtlas)

The toxin produced by the bacillus Vibrio cholerae crosses the enterocyte and elevates the messenger cyclic AMP, inhibiting sodium absorption and stimulating chloride secretion.