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Am J Physiol Gastrointest Liver Physiol 279: G757-G766, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 4, G757-G766, October 2000

Rotavirus alters paracellular permeability and energy metabolism in Caco-2 cells

Kathleen G. Dickman1,3, Scott J. Hempson1, Joseph Anderson3, Scott Lippe2, Liming Zhao2, Robert Burakoff2,3, and Robert D. Shaw1,3

1 Research Service, Department of Veterans Affairs Medical Center, Northport, 11768; 2 Department of Medicine, Winthrop University Hospital, Mineola 11501; and 3 Department of Medicine, University at Stony Brook, Stony Brook, New York 11733

Rotaviruses infect epithelial cells of the small intestine, but the pathophysiology of the resulting severe diarrhea is incompletely understood. Histological damage to intestinal epithelium is not a consistent feature, and in vitro studies showed that intestinal cells did not undergo rapid death and lysis during viral replication. We show that rotavirus infection of Caco-2 cells caused disruption of tight junctions and loss of transepithelial resistance (TER) in the absence of cell death. TER declined from 300 to 22 Omega  · cm2 between 8 and 24 h after infection and was accompanied by increased transepithelial permeability to macromolecules of 478 and 4,000 Da. Distribution of tight junction proteins claudin-1, occludin, and ZO-1 was significantly altered during infection. Claudin-1 redistribution was notably apparent at the onset of the decline in TER. Infection was associated with increased production of lactate, decreased mitochondrial oxygen consumption, and reduced cellular ATP (60% of control at 24 h after infection), conditions known to reduce the integrity of epithelial tight junctions. In conclusion, these data show that rotavirus infection of Caco-2 intestinal cells altered tight junction structure and function, which may be a response to metabolic dysfunction.

oxygen consumption; lactate; ATP; transepithelial resistance; zonula occludens; tight junctions; claudin-1; occludin


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