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Effect of E. coli heat-stable enterotoxin on colonic transport in guanylyl cyclase C receptor-deficient mice
A N Charney1, R W Egnor, J T Alexander-Chacko
1Nephrology Section, Veterans Affairs Medical Center, 423 E. 23rd Street, New York, NY 10010, USA.
Abstract:
We studied the functional importance of the colonic guanylyl cyclase C (GCC) receptor in GCC receptor-deficient mice. Mice were anesthetized with pentobarbital sodium, and colon segments were studied in Ussing chambers in HCO3- Ringer under short-circuit conditions. Receptor-deficient mouse proximal colon exhibited similar net Na+ absorption, lower net Cl- absorption, and a negative residual ion flux (J(R)), indicating net HCO3- absorption compared with that in normal mice. In normal mouse proximal colon, mucosal addition of 50 nM Escherichia coli heat-stable enterotoxin (STa) increased the serosal-to-mucosal flux of Cl- (J(s-->m)(Cl)) and decreased net Cl- flux (J(net)(Cl)) accompanied by increases in short-circuit current (I(sc)), potential difference (PD), and tissue conductance (G). Serosal STa had no effect. In distal colon neither mucosal nor serosal STa affected ion transport. In receptor-deficient mice, neither mucosal nor serosal 500 nM STa affected electrolyte transport in proximal or distal colon. In these mice, 1 mM 8-bromo-cGMP produced changes in proximal colon J(s-->m)(Cl) and J(net)(Cl), I(sc), PD, G, and J(R) similar to mucosal STa addition in normal mice. We conclude that the GCC receptor is necessary in the mouse proximal colon for a secretory response to mucosal STa.
Insights
The guanylyl cyclase C (GCC) receptor in mouse proximal colon is essential for the secretory response to E. coli heat-stable enterotoxin (STa). Without the GCC receptor, STa cannot induce electrolyte transport changes.
Area of Science:
- Physiology
- Gastroenterology
- Molecular Biology
Background:
- The colonic guanylyl cyclase C (GCC) receptor plays a role in regulating intestinal ion transport.
- Escherichia coli heat-stable enterotoxin (STa) is a known activator of intestinal secretion.
- Understanding the specific role of the GCC receptor in STa-mediated responses is crucial for elucidating mechanisms of bacterial enteritis.
Purpose of the Study:
- To investigate the functional importance of the colonic GCC receptor in mediating the secretory effects of STa.
- To compare ion transport in GCC receptor-deficient mice with that in normal mice following STa stimulation.
Main Methods:
- Utilized GCC receptor-deficient mice and normal littermates.
- Examined colon segments in Ussing chambers under short-circuit conditions.
- Measured ion fluxes (Na+, Cl-, HCO3-), short-circuit current (Isc), potential difference (PD), and tissue conductance (G).
- Administered STa and 8-bromo-cGMP to assess effects on electrolyte transport.
Main Results:
- GCC receptor-deficient mouse proximal colon showed reduced net Cl- absorption and net HCO3- absorption compared to normal mice.
- In normal mice, mucosal STa increased Cl- secretion and altered ion transport parameters.
- STa had no effect on electrolyte transport in GCC receptor-deficient mice, but 8-bromo-cGMP mimicked STa's effects, indicating the downstream pathway is intact.
Conclusions:
- The GCC receptor is indispensable in the mouse proximal colon for mediating the secretory response to mucosal STa.
- These findings highlight the critical role of the GCC receptor as the specific mediator of STa's action in the proximal colon.
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