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Mechanisms of cholera toxin-induced diarrhea

E Beubler1, R Schuligoi

  • 1Department of Experimental and Clinical Pharmacology, Karl-Franzens-University of Graz, 8010 Graz, Austria. eckhard.beubler@kfunigraz.ac.at

Annals of the New York Academy of Sciences
|February 24, 2001
PubMed

Insights

Cholera toxin utilizes prostaglandin E2 (PGE2) for its secretory effects, with cyclooxygenase-2 (COX-2) being the key enzyme in this process. Selective COX-2 inhibitors effectively reduced cholera toxin-induced fluid secretion in rats.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Pharmacology

Background:

  • Cholera pathogenesis involves mediators like cyclic adenosine monophosphate, 5-hydroxytryptamine, and prostaglandins.
  • The roles of cyclooxygenase (COX) isoforms, specifically COX-1 and COX-2, in cholera toxin's effects require further elucidation.

Purpose of the Study:

  • To investigate the specific roles of COX-1 and COX-2 in cholera toxin-induced prostaglandin E2 (PGE2) biosynthesis and fluid secretion.
  • To determine whether cholera toxin affects COX-1 and COX-2 mRNA expression in the rat jejunum.

Main Methods:

  • Utilized selective COX-2 inhibitors (NS-398 and DFU) in vivo in rat jejunum models.
  • Assessed PGE2 biosynthesis and fluid secretion following cholera toxin administration.
  • Analyzed COX-1 and COX-2 mRNA expression in mucosal scrapings using RT-PCR.
  • Investigated the effects of dexamethasone and E. coli lipopolysaccharide (LPS) on COX-2 expression.

Main Results:

  • Selective COX-2 inhibitors (NS-398, DFU) completely suppressed cholera toxin-induced PGE2 biosynthesis.
  • These inhibitors also caused a dose-dependent inhibition of cholera toxin-induced fluid secretion.
  • Cholera toxin did not alter COX-1 or COX-2 mRNA expression.
  • Dexamethasone did not affect cholera toxin-induced PGE2 or COX-2 mRNA levels, unlike its effect on LPS-induced COX-2 expression.

Conclusions:

  • Cholera toxin employs prostaglandin E2 (PGE2) as a mediator for its secretory effects.
  • Prostaglandins involved in cholera toxin's action are primarily metabolized via cyclooxygenase-2 (COX-2).
  • Cholera toxin does not induce COX-2 mRNA expression, suggesting constitutive COX-2 activity is involved.

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