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

Abstract

ABSTRACT 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, 36 Cl 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.