Glycerol supplementation enhances L. reuteri's protective effect against S. Typhimurium colonization in a 3-D model of colonic epithelium.

Glycerol supplementation enhances L. reuteri's protective effect against S. Typhimurium colonization in a 3-D model of colonic epithelium.
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补充甘油在结肠上皮的3-D模型中增强了Reuteri对伤寒链霉菌定殖的保护作用。

DOI:
10.1371/journal.pone.0037116
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Nickerson CA
Nickerson CA
中科院分区:
综合性期刊3区
文献类型:
--
作者:
De Weirdt R;Crabbé A;Roos S;Vollenweider S;Lacroix C;van Pijkeren JP;Britton RA;Sarker S;Van de Wiele T;Nickerson CA

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罗伊氏乳杆菌的益生菌作用被推测部分取决于其在肠道中甘油减少期间产生抗微生物物质罗伊素的能力。在这项研究中,这一进程的潜力,以保护人类肠上皮细胞感染沙门氏菌肠道血清型鼠伤寒进行了调查。我们使用了一个三维(3-D)的人体结肠上皮细胞的器官型模型,该模型先前已被验证并应用于研究S。鼠伤寒和肠上皮导致肠道沙门氏菌病。利用这个模型系统,我们证明了L。reuteri保护肠细胞免受沙门氏菌感染的早期阶段,当L.刺激罗伊氏细胞由甘油产生罗伊蛋白。更具体地,L.罗伊氏杆菌引起沙门氏菌粘附和侵袭(1个对数单位)和细胞内存活(2个对数单位)的减少。相比之下,L.不含罗伊氏蛋白的罗伊氏发酵物刺激细胞内沙门氏菌群体的生长,具有1个对数单位。短期暴露于reuterin或含reuterin的发酵物对肠上皮细胞健康没有观察到负面影响。然而,长期暴露(24小时)诱导上皮聚集体内的细胞-细胞接触完全丧失,并损害细胞活力。总的来说,这些结果揭示了罗伊特在抑制沙门氏菌诱导的肠道感染中的潜在作用,并可能支持甘油和L。reuteri。虽然未来的罗伊素对肠道健康的体外和体内研究应该微调我们对机制效应的理解,特别是在复杂的肠道微生物群存在的情况下,但这是第一次报告罗伊素对任何哺乳动物细胞类型中肠道感染过程的影响。
The probiotic effects of Lactobacillus reuteri have been speculated to partly depend on its capacity to produce the antimicrobial substance reuterin during the reduction of glycerol in the gut. In this study, the potential of this process to protect human intestinal epithelial cells against infection with Salmonella enterica serovar Typhimurium was investigated. We used a three-dimensional (3-D) organotypic model of human colonic epithelium that was previously validated and applied to study interactions between S. Typhimurium and the intestinal epithelium that lead to enteric salmonellosis. Using this model system, we show that L. reuteri protects the intestinal cells against the early stages of Salmonella infection and that this effect is significantly increased when L. reuteri is stimulated to produce reuterin from glycerol. More specifically, the reuterin-containing ferment of L. reuteri caused a reduction in Salmonella adherence and invasion (1 log unit), and intracellular survival (2 log units). In contrast, the L. reuteri ferment without reuterin stimulated growth of the intracellular Salmonella population with 1 log unit. The short-term exposure to reuterin or the reuterin-containing ferment had no observed negative impact on intestinal epithelial cell health. However, long-term exposure (24 h) induced a complete loss of cell-cell contact within the epithelial aggregates and compromised cell viability. Collectively, these results shed light on a potential role for reuterin in inhibiting Salmonella-induced intestinal infections and may support the combined application of glycerol and L. reuteri. While future in vitro and in vivo studies of reuterin on intestinal health should fine-tune our understanding of the mechanistic effects, in particular in the presence of a complex gut microbiota, this the first report of a reuterin effect on the enteric infection process in any mammalian cell type.
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