Chloride secretion, enterocytes

Although infection with C. parvum is considered predominantly secretory, histopathologic studies have revealed varying degrees of villous atrophy and infiltration of inflammatory cells beneath the epithelial mucosa [85, 86], Prostaglandins, which are known to induce cAMP-mediated apical chloride secretion and inhibit electroneutral sodium chloride and water absorption in enterocytes, have been demonstrated to be elevated in a porcine model of cryptosporidiosis [87], Inflammatory cytokines such as IL-1, IL-8 and TNF-a are induced in intestinal epithelial cell lines infected with Cryptosporidium and in animal models of cryptosporidiosis and have been postulated to play a role in pathogenesis [88, 89], Expression of TNF-a and IL-1 mRNA in the majority of jejunal biopsies of adult volunteers after experimental infection were also observed, although this did not correlate with the enteric symptoms [90]. 

After being ingested, the V. cholerae organisms attach to the brash border of the intestinal epithelium and secrete an exotoxin that binds irreversibly to a specific chemical receptor (Gmi ganglioside) on the cell surface. This exotoxin catalyzes an ADP-ribosylation reaction that increases adenylate cyclase activity and thus cAMP levels in the enterocyte. As a result, the normal absorption of sodium, anions, and water from the gut lumen into the intestinal cell is markedly diminished. The exotoxin also stimulates the crypt cells to secrete chloride, accompanied by cations... 

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