Background. Lactobacillus shows beneficial anti-inflammatory effects on Salmonella infection. The maintenance of the tight junction (TJ) integrity plays an importance role in avoiding bacterial invasion. Whether Lactobacillus could be used to regulate the TJ protein expression and distribution in inflamed intestinal epithelial cells was determined. Methods. Using the transwell coculture model, Salmonella lipopolysaccharide (LPS) was apically added to polarized Caco-2 cells cocultured with peripheral blood mononuclear cells in the basolateral compartment. LPS-stimulated Caco-2 cells were incubated with various Lactobacillus strains. TJ integrity was determined by measuring transepithelial electrical resistance across Caco-2 monolayer. Expression and localization of TJ proteins (zonula-occludens- (ZO-) 1) were determined by Western blot and immunofluorescence microscopy. Results. Various strains of Lactobacillus were responsible for the different modulations of cell layer integrity. LPS was specifically able to disrupt epithelial barrier and change the location of ZO-1. Our data demonstrate that Lactobacillus could attenuate the barrier disruption of intestinal epithelial cells caused by Salmonella LPS administration. We showed that Lactobacillus strains are associated with the maintenance of the tight junction integrity and appearance. Conclusion. In this study we provide insight that live probiotics could improve epithelial barrier properties and this may explain the potential mechanism behind their beneficial effect in vivo. 1. Introduction Salmonella infection is a common cause of human food poisoning worldwide and can induce a broad spectrum of diseases from mild diarrhea to typhoid. All Salmonella serotypes share the ability to gain entry to the host through oral ingestion of contaminated food or water. They induce their own uptake into intestinal epithelial by Salmonella pathogenicity island-1 (SPI-1) type 3 secretion system. This epithelial barrier function can be further weakened by infection with bacteria, including S. typhimurium effectors [1, 2]. Salmonella enterica serovar Typhimurium has developed means of breaching the mucosal epithelial barrier by usurping signaling mechanisms within host cells [3]. It is likely that Salmonella induces localized effects on tight junction permeability during intestinal infections. These effects may act synergistically with other conditions, such as inflammatory responses, to promote tight junction (TJ) dysfunction [4]. At present, S. typhimurium overcoming the intestinal barrier is the most widely accepted
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