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. 1988 Aug;82(2):514–523. doi: 10.1172/JCI113626

Mechanism of action of Escherichia coli heat stable enterotoxin in a human colonic cell line.

P A Huott 1, W Liu 1, J A McRoberts 1, R A Giannella 1, K Dharmsathaphorn 1
PMCID: PMC303542  PMID: 2457034

Abstract

Escherichia coli heat stable enterotoxin (STa) caused Cl- secretion across T84 cell monolayers in a dose-dependent manner only when applied to the apical membrane surface and not when applied to the basolateral surface. Measurement of cAMP, cGMP, and free cytosolic Ca2+ in response to STa suggested that cGMP alone mediated the Cl- secretory response. Studies utilizing blockers of the Na+,K+-ATPase pump, a Na+,K+,Cl- cotransport system, a K+ channel, and a Cl- channel suggest that all of them participate in the Cl- secretory process induced by STa. The results suggest that the Cl- secretory response induced by STa is mediated by cGMP after the enterotoxin binds to its receptor on the apical membrane. The enterotoxin, by increasing cGMP, opens a K+ channel on the basolateral membrane as well as a Cl- channel on the apical membrane. The activation of these ion exit mechanisms, together with activations of the Na+,K+,Cl- cotransporter and the Na+,K+-ATPase pump drives Cl- exit through the Cl- channel on the apical membrane.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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