These proteins are considered to be involved in the regulation of paracellular permeability. The TJ effect can be documented by reduction in transepithelial electrical resistance (TER). Some bacterial pathogens manipulate the apical-junctional complex from the apical surface. The cellular cascade induced in Enteropathogenic Escherichia coli (EPEC) infection, which leads to decrease in TER, is not well understood. One such strategy is to target the regulatory elements of the actin cytoskeleton. EPEC infects the apical surface of intestinal epithelial cells and modifies the actin cytoskeleton

by GSK3326595 forming actin-rich pedestals beneath the attached bacteria, firmly anchoring the bacterium to the host cell [5]. Changes in the host cell actin cytoskeleton could lead to a loss of absorptive surfaces in intestinal epithelial cells and account for the persistent diarrhea often associated NVP-LDE225 cell line with EPEC infection. Control of perijunctional actin may be also the final effector mechanism in modulating paracellular permeability

[6]. It is increasingly recognized that Lactobacillus plantarum (L. plantarum) has the ability to protect against EPEC-induced damage of the epithelial monolayer barrier function by preventing changes in host cell morphology, attaching/effacing (A/E) lesion formation, monolayer resistance, and macromolecular permeability [7–10]. In recent years, Moorthy G et al [11] evaluated the effect of L. rhamnosus and L. acidophilus on the maintenance of intestinal membrane integrity during S. dysenteriae 1-induced diarrhea in rats. They found that induced rats showed a significant reduction Endonuclease in the membrane-bound ATPases and reduced expression of TJ proteins in the membrane, coupled with their increased expression in the cytosol, indicating membrane damage. Transmission electron microscopic studies correlated with biochemical parameters. Pretreatment with combination of L. rhamnosus and L. acidophilus significantly prevented these changes. However, the

cellular mechanism involved in this protective effect still remained to be clarified. The aim of this study was to investigate the molecular mechanisms underlying the beneficial effects of the L. plantarum. Moreover, as infections with Enteroinvasive Escherichia coli (EIEC) were accompanied by the disruption of epithelial integrity was also asked whether the presence of L. plantarum would influence the otherwise deleterious barrier disruption of caco-2 cells caused by EIEC bacteria. The permeability, the distribution and expression of tight junction proteins (such as Claudin-1, Occludin, JAM-1 and ZO-1) and the cytoskeleton were examined when infected with EIEC or NU7441 ic50 adhesived of L. plantarum after infection. Results L.