American Journal of Clinical Nutrition, Vol 32, 189-196, Copyright © 1979 by The American Society for Clinical Nutrition, Inc

REVIEW ARTICLES

Mechanisms of action of cholera and Escherichia coli enterotoxins

M Field

Current information is reviewed on the mechanism of secretion in small intestine, including how it is altered by cyclic 3',5'-adenosine monophosphate and on the structures and properties of cholera and both heat-labile and heat-stable Escherichia coli enterotoxins. Two separate active ion transport processes are altered by cyclic 3',5'-adenosine monophosphate: 1) coupled absorption of NaCl is inhibited in villus cells and 2) active anion secretion is stimulated, probably in crypt cells. Cholera and heat-labile E. coli toxins exert their secretory effect by stimulating intestinal mucosal adenylate cyclase. This stimulation results from the A1 subunit catalyzed transfer of adenosine diphosphate ribose from NAD to a membrane-bound guanosine triphosphatase, thereby inhibiting the enzyme, which normally represses adenylate cyclase. Heat-stable E. coli enterotoxin stimulates intestinal mucosal guanylate cyclase, which appears to be the basis for its enterotoxicity.

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