Intestinal adaptation to cyclic AMP-mediated hypersecretion induced by the heat-labile enterotoxin of Vibrio cholerae and Escherichia coli.
Adaptation to cholera toxin (CT) and the heat-labile enterotoxin (LT) from E. coli is studied in vivo in the rat small intestine. Repeated peroral pretreatment with CT or LT induces protracted inhibition of the intestinal fluid response to these toxins. The CT-induced mucus release from intestinal goblet cells is not influenced by CT pretreatment and the binding of CT to the epithelium remains intact. However, the adenylate cyclase activity, which mediates CT and LT action, is repressed--as judged from the response of this enzyme to both CT, LT and prostaglandin E1. The results suggests that protection against CT and LT acquired in the gut is achieved by desensitization of the adenylate cyclase system.
D000262:Adenylyl Cyclases / Q000032:analysis; D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity*; D002772:Cholera Toxin / Q000378:metabolism / Q000633:toxicity*; D000242:Cyclic AMP / Q000502:physiology*; D004768:Enterotoxins / Q000633:toxicity*; D029968:Escherichia coli Proteins; D007419:Intestinal Secretions / Q000187:drug effects*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D001427:Bacterial Toxins; D004768:Enterotoxins; D029968:Escherichia coli Proteins; D002772:Cholera Toxin; C027538:heat-labile enterotoxin, E coli; D000242:Cyclic AMP; D000262:Adenylyl Cyclases