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J. Virol. doi:10.1128/JVI.00263-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

A protein kinase A-dependent mechanism by which rotavirus affects in human differentiated intestinal Caco-2 cells the distribution and the mRNA level of the functional tight junction-associated protein, occludin

INSERM, UMR 756, Châtenay-Malabry, France. Université Paris-Sud, Faculté de Pharmacie, Châtenay-Malabry, France

^* To whom correspondence should be addressed. Email: alain.servin{at}u-psud.fr.

	Abstract

We showed that at the tight junctions (TJs) of Caco-2 cell monolayers, Rhesus monkey rotavirus (RRV) infection induced the disappearance of occludin. Confocal laser scanning microscopy (CLSM) showed the disappearance of occludin from the cell-cell boundaries without modifying the expression of the other TJs-associated proteins, ZO-1 and ZO-3. Western immunoblot analysis in RRV-infected cells showed a significant fall in the levels of the non-phosphorylated form of occludin in both Triton X100-insoluble and Triton X100-soluble fractions, without any change in the levels of the phosphorylated form of occludin. Quantitative reverse transcription polymerase chain reactions revealed that the level of transcription of the gene encoding for occludin was significantly reduced in RRV-infected cells. Treatment of RRV-infected cells with Rp-cAMP and PKA inhibitors, H89 and KT5720 during the time-course of the infection restored the distribution of occludin and a normal level of transcription of the gene encoding for occludin.