Fig 1.

Movement of sodium ions (Na⁺) and chloride ions (Cl⁻) in the small intestine during health and diarrhoea. (a) Normal subjects. Na⁺ is absorbed by two different mechanisms in absorptive cells from villi: glucose-stimulated absorption and electroneutral absorption (which represents the coupling of Na/H and Cl/bicarbonate (HCO₃) exchanges). (b) During diarrhoea caused by a toxin and inflammation. In toxigenic diarrhoea (eg caused by the enterotoxin produced by Vibrio cholerae), increased mucosal levels of cyclic adenosine monophosphate (cAMP) inhibit electroneutral sodium chloride (NaCl) absorption but have no effect on glucose-stimulated Na⁺ absorption. In inflammatory diarrhoea (eg following infection with Shigella spp or Salmonella spp) there is extensive histological damage, resulting in altered cell morphology and reduced glucose-stimulated Na⁺ and electroneutral NaCl absorption. The role of one or more cytokines in this inflammatory response is critical. In secretory cells from crypts, Cl⁻ secretion is minimal in normal subjects and activated by cAMP in toxigenic and inflammatory diarrhoea. Reproduced from reference 1.