Rotavirus-Induced Structural and Functional Alterations in Tight Junctions of Polarized Intestinal Caco-2 Cell Monolayers

AUTOR(ES)

Obert, Guillaume

FONTE

American Society for Microbiology

RESUMO

We provide here new insights into rotavirus (RRV) pathogenicity by showing that RRV infection promotes structural and functional injuries localized at the tight junctions (TJ) in the cell-cell junctional complex of cultured polarized human intestinal Caco-2 cells forming monolayers. RRV infection resulted in a progressive increase in the paracellular permeability to [3H]mannitol as a function of the time postinfection. We observed a disorganization of the TJ-associated protein occludin as a function of the time postinfection, whereas distribution of the zonula adherens associated E-cadherin was not affected. These structural and functional RRV-induced TJ injuries were not accompanied by alteration in cell and monolayer integrity, as assessed by the lack of change in transepithelial membrane resistance and lactate dehydrogenase release. Finally, using the stabilizer of actin filaments Jasplakinolide, we demonstrated that the RRV-induced structural and functional alterations in TJ are independent of the RRV-induced apical F-actin rearrangements.

Documentos Relacionados

• Adherence to and Penetration of Human Intestinal Caco-2 Epithelial Cell Monolayers by Pseudomonas aeruginosa
• Butyrate Enhances the Intestinal Barrier by Facilitating Tight Junction Assembly via Activation of AMP-Activated Protein Kinase in Caco-2 Cell Monolayers12
• Rotavirus-induced fusion from without in tissue culture cells.
• Heterologous protection against rotavirus-induced disease in gnotobiotic piglets.
• Entamoeba histolytica interactions with polarized human intestinal Caco-2 epithelial cells.