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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Role of Intestinal Epithelial Cells in Immune Effects Mediated by Gram-Positive Probiotic Bacteria: Involvement of Toll-Like Receptors
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Role of Intestinal Epithelial Cells in Immune Effects Mediated by Gram-Positive Probiotic Bacteria: Involvement of Toll-Like Receptors

机译：肠道上皮细胞在革兰氏阳性益生菌介导的免疫作用中的作用：类似收费受体的参与。

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The mechanisms by which probiotic bacteria exert their effects on the immune system are not completely understood, but the epithelium may be a crucial player in the orchestration of the effects induced. In a previous work, we observed that some orally administered strains of lactic acid bacteria (LAB) increased the number of immunoglobulin A (IgA)-producing cells in the small intestine without a concomitant increase in the CD4+ T-cell population, indicating that some LAB strains induce clonal expansion only of B cells triggered to produce IgA. The present work aimed to study the cytokines induced by the interaction of probiotic LAB with murine intestinal epithelial cells (IEC) in healthy animals. We focused our investigation mainly on the secretion of interleukin 6 (IL-6) necessary for the clonal expansion of B cells previously observed with probiotic bacteria. The role of Toll-like receptors (TLRs) in such interaction was also addressed. The cytokines released by primary cultures of IEC in animals fed with Lactobacillus casei CRL 431 or Lactobacillus helveticus R389 were determined. Cytokines were also determined in the supernatants of primary cultures of IEC of unfed animals challenged with different concentrations of viable or nonviable lactobacilli and Escherichia coli, previously blocked or not with anti-TLR2 and anti-TLR4. We concluded that the small intestine is the place where a major distinction would occur between probiotic LAB and pathogens. This distinction comprises the type of cytokines released and the magnitude of the response, cutting across the line that separates IL-6 necessary for B-cell differentiation, which was the case with probiotic lactobacilli, from inflammatory levels of IL-6 for pathogens.
机译：益生菌对免疫系统发挥作用的机制尚不完全清楚，但上皮可能是协调诱导作用的关键因素。在以前的工作中，我们观察到一些口服的乳酸菌菌株（LAB）可增加小肠中产生免疫球蛋白A（IgA）的细胞数量，而CD4 + 却不会随之增加。 T细胞种群，表明某些LAB菌株仅诱导触发产生IgA的B细胞的克隆扩增。本工作旨在研究健康动物中益生菌LAB与鼠肠上皮细胞（IEC）相互作用诱导的细胞因子。我们的研究主要集中在分泌白细胞介素6（IL-6）的分泌上，而白细胞介素6（IL-6）是以前用益生菌观察到的B细胞克隆扩增所必需的。还探讨了Toll样受体（TLR）在此类相互作用中的作用。测定了由干酪乳杆菌CRL 431或瑞士乳杆菌R389饲喂的动物的IEC原代培养物释放的细胞因子。还测定了未食用动物的IEC原代培养物上清液中的细胞因子，这些动物受到不同浓度的存活或不存活的乳酸杆菌和大肠杆菌的攻击，这些细菌先前已被抗-TLR2和抗-TLR4阻断。我们得出的结论是，小肠是益生菌LAB与病原体之间主要区别的地方。这种区别包括释放的细胞因子的类型和响应的大小，跨越了区分B细胞分化所必需的IL-6（对于益生菌乳酸菌而言）和针对病原体的IL-6的炎性水平。

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