Dataset for: <i>Lactobacillus reuteri </i>strains protect epithelial barrier integrity of IPEC-J2 monolayers from the detrimental effect of Enterotoxigenic <i>Escherichia coli</i> (ETEC).
2018-01-25T07:17:01Z (GMT) by
<i>Lactobacillus reuteri</i> is an inhabitant of the gastrointestinal (GI) tract of mammals and birds and several strains of this species are known to be effective probiotics. The mechanisms by which <i><i>L. reuteri</i></i> confers its health-promoting effects are far from being fully understood, but protection of the mucosal barrier is thought to be important. Leaky gut is a state of abnormal intestinal permeability with implications for the pathophysiology of various gastrointestinal disorders. Enterotoxigenic<i><i> Escherichia coli </i></i>(ETEC) can invade the intestinal mucosa and induce changes in barrier function by producing enterotoxin or by direct invasion of the intestinal epithelium.Our hypothesis was that<i> L. reuteri </i>can protect the mucosal barrier, and the goal of the study was to challenge this hypothesis by monitoring the protective effect of <i>L. reuteri </i>strains on epithelial dysfunction caused by ETEC. This study examined the potential of <i><i>Lactobacillus reuteri</i></i> to attenuate the effect of ETEC strain 853/67 on mucosal permeability. Using an infection model based on the porcine intestinal cell line IPEC-J2, it was demonstrated that pre-treatment of the cells with human-derived <i>L. reuteri </i>strains (ATCC PTA 6475, DSM 17938 and 1563F) and a rat strain (R2LC) reduced the detrimental effect of ETEC in a dose-dependent manner, as monitored by permeability of FITC-dextran and transepithelial electrical resistance (TEER). Moreover, the results revealed that ETEC up-regulated pro-inflammatory cytokines IL-6 and TNFα and decreased expression of the shorter isoform of ZO-1 (187 kDa) and E-cadherin. In contrast, pre-treatment with<i> L. reuteri</i> DSM 17938 and 1563F downregulated expression of IL-6 and TNFα, and led to an increase in production of the longer isoform of ZO-1 (195 kDa) and maintained E-cadherin expression. Interestingly, expression of ZO-1 (187 kDa) was preserved only when the infected cells were pre-treated with strain 1563F. These findings demonstrate that <i><i>L. reuteri</i></i> strains exert a protective effect against ETEC-induced mucosal integrity disruption.