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Research Article Free access | 10.1172/JCI113626

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

P A Huott, W Liu, J A McRoberts, R A Giannella, and K Dharmsathaphorn

Department of Medicine, San Diego Medical Center, California 92103.

Find articles by Huott, P. in: PubMed | Google Scholar

Department of Medicine, San Diego Medical Center, California 92103.

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Department of Medicine, San Diego Medical Center, California 92103.

Find articles by McRoberts, J. in: PubMed | Google Scholar

Department of Medicine, San Diego Medical Center, California 92103.

Find articles by Giannella, R. in: PubMed | Google Scholar

Department of Medicine, San Diego Medical Center, California 92103.

Find articles by Dharmsathaphorn, K. in: PubMed | Google Scholar

Published August 1, 1988 - More info

Published in Volume 82, Issue 2 on August 1, 1988
J Clin Invest. 1988;82(2):514–523. https://doi.org/10.1172/JCI113626.
© 1988 The American Society for Clinical Investigation
Published August 1, 1988 - Version history
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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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