Abstract
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 language | English (US) |
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Pages (from-to) | C567-C577 |
Journal | American Journal of Physiology - Cell Physiology |
Volume | 279 |
Issue number | 3 48-3 |
DOIs | |
State | Published - 2000 |
Keywords
- Accessory cholera enterotoxin
- Bacterial pathogenesis
- Bacterial toxin
- Cholera
- Second messenger
- Ussing chamber
ASJC Scopus subject areas
- Physiology
- Cell Biology