Intestinal ion and nutrient transport in health and infectious diarrhoeal diseases.

Absorption of water from the intestine occurs in response to the osmotic gradient as a passive consequence of the active transfer of solutes (nutrients and electrolytes, with Na absorption playing a key role) from the intestinal lumen to the serosal side. During intestinal infections, several possible derangements of such a situation may occur, ultimately leading to the shift of net water absorption to secretion and, thus, to diarrhoea. In rotaviral diarrhoea, the mature enterocytes are invaded by the virus and exfoliate, thus inducing villous atrophy and crypt hyperplasia. Consequently, undigested and unabsorbed nutrients cause an osmolar diarrhoea, while the ongoing process of crypt secretion contributes by adding active anion and water secretion. In bacterial intestinal infections, the pathogenetic mechanisms are essentially mucosal invasion, adherence, cytotoxicity or release of enterotoxins. The pathophysiology of bacterial diarrhoea is best known for the latter mechanism; heat-labile and heat-stable families of enterotoxins have been described and characterised that act by inducing, respectively, an increase in the enterocyte's cyclic AMP or cyclic GMP content. Such alteration leads, in a morphologically intact mucosa, to changes in the major electrolyte transport processes that reverse net absorption of ions and water to net secretion and thus to secretory diarrhoea. As for nutrient absorption, although experimental evidence indicates an impairment of glucose and amino acid absorption in rotaviral diarrhoea, many clinical trials have shown the successful use of oral rehydration solutions in such circumstances. The same applies to bacterial-induced diarrhoeas; the well-established observation that, in enterotoxic diarrhoea of all kinds, the coupled transport of Na and nutrients such as glucose or amino acids is intact has proved to be the cornerstone of the highly successful, widespread use of oral rehydration solutions.