Vibrio cholerae ACE stimulates Ca2+-dependent Cl-/HCO3- secretion in T84 cells in vitro

Michele Trucksis, Timothy L. Conn, Steven S. Wasserman, Cynthia L. Sears

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


ACE, accessory cholera enterotoxin, the third enterotoxin in Vibrio cholerae, has been reported to increase short-circuit current (I(sc)) in rabbit ileum and to cause fluid secretion in ligated rabbit ileal loops. We studied the ACE-induced change in I(sc) and potential difference (PD) in T84 monolayers mounted in modified Ussing chambers, an in vitro model of a Cl- secretory cell. ACE added to the apical surface alone stimulated a rapid increase in I(sc) and PD that was concentration dependent and immediately reversed when the toxin was removed. Ion replacement studies established that the current was dependent on Cl- and HCO3/-. ACE acted synergistically with the Ca2+-dependent acetylcholine analog, carbachol, to stimulate secretion in T84 monolayers. In contrast, the secretory response to cAMP or cGMP agonists was not enhanced by ACE. The ACE-stimulated secretion was dependent on extracellular and intracellular Ca2+ but was not associated with an increase in intracellular cyclic nucleotides. We conclude that the mechanism of secretion by ACE involves Ca2+ as a second messenger and that this toxin stimulates a novel Ca2+-dependent synergy.

Original languageEnglish (US)
Pages (from-to)C567-C577
JournalAmerican Journal of Physiology - Cell Physiology
Issue number3 48-3
StatePublished - 2000


  • Accessory cholera enterotoxin
  • Bacterial pathogenesis
  • Bacterial toxin
  • Cholera
  • Second messenger
  • Ussing chamber

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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