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).

<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.

罗伊氏乳杆菌（Lactobacillus reuteri）是栖息于哺乳动物与鸟类胃肠道（gastrointestinal tract, GI）的正常菌群成员，该物种的多个菌株已被证实为有效的益生菌。罗伊氏乳杆菌发挥健康促进作用的机制尚未完全阐明，但维护黏膜屏障被认为是关键机制之一。
肠漏（leaky gut）是一种肠道通透性异常的病理状态，与多种胃肠道疾病的病理生理学过程密切相关。产肠毒素性大肠杆菌（Enterotoxigenic Escherichia coli, ETEC）可侵袭肠黏膜，并通过产生肠毒素或直接侵入肠上皮细胞，引发屏障功能异常。
本研究提出假设：罗伊氏乳杆菌可维护肠黏膜屏障，研究目的即通过监测罗伊氏乳杆菌菌株对ETEC诱导的上皮功能障碍的保护作用，验证该假说。
本研究探究了罗伊氏乳杆菌减弱产肠毒素性大肠杆菌菌株853/67对黏膜通透性影响的潜力。采用基于猪肠道细胞系IPEC-J2的感染模型，实验证实：经人类来源的罗伊氏乳杆菌菌株（ATCC PTA 6475、DSM 17938与1563F）以及大鼠来源菌株R2LC预处理细胞，可通过剂量依赖性方式减轻ETEC带来的损伤效应，该效应通过FITC-葡聚糖（FITC-dextran）通透性检测与跨上皮电阻（transepithelial electrical resistance, TEER）得以验证。
此外，研究结果显示，ETEC可上调促炎细胞因子白细胞介素6（Interleukin 6, IL-6）与肿瘤坏死因子α（Tumor Necrosis Factor-α, TNF-α）的表达，同时下调紧密连接蛋白1（Zonula Occludens 1, ZO-1）短亚型（187 kDa）以及上皮型钙粘蛋白（E-cadherin）的表达水平。与之相反，经罗伊氏乳杆菌DSM 17938与1563F预处理的细胞，可下调IL-6与TNF-α的表达，促进ZO-1长亚型（195 kDa）的产生，并维持上皮型钙粘蛋白的表达。
值得注意的是，仅当感染细胞经菌株1563F预处理时，ZO-1（187 kDa）的表达才得以保留。上述研究结果表明，罗伊氏乳杆菌菌株可对抗ETEC诱导的黏膜完整性破坏，发挥黏膜保护作用。