Rotavirus Infection Stimulates the Cl− Reabsorption Process across the Intestinal Brush-Border Membrane of Young Rabbits

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American Society for Microbiology

RESUMO

Rotavirus is a major cause of infantile gastroenteritis worldwide. However, the mechanisms underlying fluid and electrolyte secretion associated with diarrhea remain largely unknown. We investigated the hypothesis that loss of Cl− into the luminal contents during rotavirus infection may be caused by a dysfunction in the chloride absorptive capacity across the intestinal brush-border membrane (BBM). The luminal Cl− concentrations in the entire small intestine of young rabbits infected with lapine rotavirus decreased at 1 and 2 days postinfection (dpi), indicating net Cl− absorption. At 7 dpi, luminal Cl− concentrations were slightly increased, indicating a moderate net Cl− secretion. By using a rapid filtration technique, 36Cl uptake across BBM was quantified by modulating the alkali-metal ion, electrical, chloride, and/or proton gradients. Rotavirus infection caused an identical, 127% ± 24% increase in all Cl− uptake activities (Cl−/H+ symport, Cl− conductance, and Cl−/anion exchange) observed across the intestinal BBM. The rotavirus activating effects on the symporter started at 1 dpi and persisted up to 7 dpi. Kinetic analyses revealed that rotavirus selectively affected the capacity parameter characterizing the symporter. We report the novel observation that rotavirus infection stimulated the Cl− reabsorption process across the intestinal BBM. We propose that the massive Cl− reabsorption in villi could partly overwhelm chloride secretion in crypt cells, which possibly increases during rotavirus diarrhea, the resulting imbalance leading to a moderate net chloride secretion.

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