Immunobiotics have emerged as a promising intervention to alleviate intestinal damage in inflammatory bowel disease (IBD). However, the beneficial properties of immunobiotics are strain dependent and, therefore, each strain has to be evaluated in order to demonstrate its potential application in IBD. Our previous in vitro and in vivo studies demonstrated that Lactobacillus jensenii TL2937 attenuates gut acute inflammatory response triggered by Toll-like receptor 4 activation. However, its effect on colitis has not been evaluated before. In this work, we studied whether the TL2937 strain was able to protect against the development of colitis in a dextran sodium sulfate (DSS)-induced mouse model and we delved into the mechanisms of action by evaluating the effect of the immunobiotic bacteria on the transcriptomic response of DSS-challenged intestinal epithelial cells. L. jensenii TL2937 was administered to adult BALB/c mice before the induction of colitis by the administration of DSS. Colitis and the associated inflammatory response were evaluated for 14 days. Mice fed with L. jensenii TL2937 had lower disease activity index and alterations of colon length when compared to control mice. Reduced myeloperoxidase activity, lower production of pro-inflammatory (TNF-α, IL-1, CXCL1, MCP-1, IL-15, and IL-17), and higher levels of immunoregulatory (IL-10 and IL-27) cytokines were found in the colon of TL2937-treated mice. In addition, the treatment of porcine intestinal epithelial (PIE) cells with L. jensenii TL2937 before the challenge with DSS differentially regulated the activation of the JNK pathway, leading to an increase in epithelial cell integrity and to a differential immunotranscriptomic response. TL2937-treated PIE cells had a significant reduction in the expression of inflammatory cytokines (TNF-α, IL-1α, IL-1β, IL-6, IL-15), chemokines (CCL2, CCL4, CCL8, CXCL4, CXCL5, CXCL9, CXCL10), adhesion molecules (SELE, SELL, EPCAM), and other immune factors (NCF1, NCF2, NOS2, SAA2) when compared to control cells after the challenge with DSS. The findings of this work indicate that (a) L. jensenii TL2937 is able to alleviate DSS-induced colitis suggesting a potential novel application for this immunobiotic strain, (b) the modulation of the transcriptomic response of intestinal epithelial cells would play a key role in the beneficial effects of the TL2937 strain on colitis, and (c) the in vitro PIE cell immunoassay system could be of value for the screening and selection of new immunobiotic strains for their application in IBD.

免疫抗生素已成为减轻炎症性肠病（IBD）肠道损伤的一种有前景的干预措施。然而，免疫抗生素的有益特性取决于菌株，因此必须对每种菌株进行评估，以证明其在 IBD 中的潜在应用。我们之前的体外和体内研究表明，詹氏乳杆菌 TL2937 可以减弱由 Toll 样受体 4 激活引发的肠道急性炎症反应。然而，之前尚未评估过它对结肠炎的作用。在这项工作中，我们研究了 TL2937 菌株是否能够在葡聚糖硫酸钠 (DSS) 诱导的小鼠模型中预防结肠炎的发展，并通过评估免疫细菌对转录组的影响来深入研究其作用机制。 DSS 攻击的肠上皮细胞的反应。在通过给予 DSS 诱导结肠炎之前，将詹氏乳杆菌 TL2937 给予成年 BALB/c 小鼠。对结肠炎和相关炎症反应进行为期 14 天的评估。与对照小鼠相比，饲喂詹氏乳杆菌 TL2937 的小鼠的疾病活动指数和结肠长度变化较低。髓过氧化物酶活性降低，促炎细胞因子（TNF-α、IL-1、CXCL1、MCP-1、IL-15 和 IL-17）产生减少，免疫调节细胞因子（IL-10 和 IL-27）水平升高在 TL2937 治疗小鼠的结肠中发现。此外，在用 DSS 攻击之前用詹氏乳杆菌 TL2937 处理猪肠上皮 (PIE) 细胞可差异调节 JNK 通路的激活，导致上皮细胞完整性增加和差异免疫转录组反应。 TL2937处理的PIE细胞炎症细胞因子（TNF-α、IL-1α、IL-1β、IL-6、IL-15）、趋化因子（CCL2、CCL4、CCL8、CXCL4、CXCL5、CXCL9）的表达显着降低、CXCL10）、粘附分子（SELE、SELL、EPCAM）和其他免疫因子（NCF1、NCF2、NOS2、SAA2）与 DSS 攻击后的对照细胞相比。这项工作的结果表明，(a) L. jensenii TL2937 能够缓解 DSS 诱导的结肠炎，表明该免疫菌株具有潜在的新应用，(b) 肠上皮细胞转录组反应的调节将发挥关键作用TL2937菌株对结肠炎的有益作用，以及（c）体外PIE细胞免疫测定系统对于筛选和选择新的免疫菌株用于IBD治疗具有重要价值。