1970
DOI: 10.1073/pnas.67.2.851
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Elevated Concentration of Adenosine 3′:5′-Cyclic Monophosphate in Intestinal Mucosa after Treatment with Cholera Toxin

Abstract: Abstract. A heat-labile factor in cell-free filtrate of a Vibrio cholerae culture induces a marked rise in the wet-weight concentration of adenosine 3': 5'-cyclic monophosphate (cyclic AMP) in the intestinal mucosa of the dog. The increase becomes appreciable 1-1.5 hr after intraluminal administration of the filtrate, about the same time as the onset of intestinal secretion in response to a heat-labile enterotoxin in the filtrate. These results are consistent with the hypothesis that cyclic AMP may be an inter… Show more

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Cited by 201 publications
(77 citation statements)
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“…In contrast, purified toxin B does not cause fluid secretion, inflammatory infiltrate, or morphologic damage in rabbit or hamster intestine (1)(2)(3). The effects of toxin A are not accompanied by elevation of adenylate cyclase (4), indicating that its mechanism of action differs from, cholera toxin and Escherichia coli heat labile enterotoxin, which stimulate intestinal adenylate cyclase and cause fluid secretion without producing an inflammatory infiltrate (5,6).…”
Section: Introductionmentioning
confidence: 99%
“…In contrast, purified toxin B does not cause fluid secretion, inflammatory infiltrate, or morphologic damage in rabbit or hamster intestine (1)(2)(3). The effects of toxin A are not accompanied by elevation of adenylate cyclase (4), indicating that its mechanism of action differs from, cholera toxin and Escherichia coli heat labile enterotoxin, which stimulate intestinal adenylate cyclase and cause fluid secretion without producing an inflammatory infiltrate (5,6).…”
Section: Introductionmentioning
confidence: 99%
“…Drawing adapted from Russel (1998) and Sandkvist (2001). masi et al 1979) to activate host cell adenylate cyclase (Cassel and Selinger 1977;Cassel and Pfeuffer 1978;Gill and Meren 1978), resulting in massive diarrhea (Greenough et al 1970;Schafer et al 1970;Sharp and Hynie 1971;Field et al 1972). E. coli enterotoxin (LT), Shigella dysenteriae shiga toxin, and E. coli shiga-like toxins are composed of a similar structural assembly (AB toxins), albeit that the mode of action for shiga toxins is to prevent ribosomal translation of host cells (Schmitt et al 1999).…”
Section: Type II Secretion Type Iv Pili and Filamentous Phagementioning
confidence: 99%
“…It has been well-established that the mechanism for orally or locally cholera enterotoxin-induced intestinal hypersecretion of water and electrolyte is an activation of adenyl cyclase activity of mucosal cells [12][13][14][15]. However, the question as to why iv injection of the same caused by the applied techniques for cAMP determination, but rather by the renal excretion of large and varying amounts of cAMP in the urine [20,21] in order to maintain a relatively constant plasma cAMP concentration.…”
Section: Discussionmentioning
confidence: 96%
“…According to the present findings, the process of cellular internalization of cholera toxin should not be considered uniform in different body cells. The selectivity for cholera toxin penetrating into the cell may be the key factor for an increased activity of adenyl cyclase, which in turn produces cAMP from ATP within the cell [12][13][14][15].…”
Section: Discussionmentioning
confidence: 99%