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INTESTINAL ADAPTATION TO CYCLIC AMP‐MEDIATED HYPERSECRETION INDUCED BY THE HEAT‐LABILE ENTEROTOXIN OF VIBRIO CHOLERAE AND ESCHERICHIA COLI
Author(s) -
LöNNROTH IVAR,
HANSSON HANSARNE,
LANGE STEFAN
Publication year - 1984
Publication title -
acta pathologica microbiologica scandinavica series b: microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0180
DOI - 10.1111/j.1699-0463.1984.tb02793.x
Subject(s) - cholera toxin , adenylate kinase , enterotoxin , cyclase , vibrio cholerae , heat stable enterotoxin , escherichia coli , microbiology and biotechnology , in vivo , chemistry , prostaglandin e , prostaglandin , enzyme , small intestine , heat labile enterotoxin , biology , biochemistry , bacteria , genetics , gene
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 E 1 . The results suggests that protection against CT and LT acquired in the gut is achieved by desensitization of the adenylate cyclase system.