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膳食低聚果糖可使大鼠体内沙门氏菌的易位呈剂量依赖性增加。

Dietary fructo-oligosaccharides dose-dependently increase translocation of salmonella in rats.

作者信息

Ten Bruggencate Sandra J M, Bovee-Oudenhoven Ingeborg M J, Lettink-Wissink Mischa L G, Van der Meer Roelof

机构信息

Nutrition and Health Program, Wageningen Center for Food Sciences/NIZO Food Research, Ede, The Netherlands.

出版信息

J Nutr. 2003 Jul;133(7):2313-8. doi: 10.1093/jn/133.7.2313.

Abstract

Prebiotics, such as fructo-oligosaccharides (FOS), stimulate the protective gut microflora, resulting in an increased production of organic acids. This may result in increased luminal killing of acid-sensitive pathogens. However, host defense against invasive pathogens, like salmonella, also depends on the barrier function of the intestinal mucosa. Rapid fermentation of prebiotics leading to high concentrations of organic acids may impair the barrier function. Therefore, we determined the dose-dependent effect of dietary FOS on the resistance of rats to Salmonella enteritidis. Male Wistar rats were fed restricted quantities of a "humanized" purified diet supplemented with 0, 3 or 6 g/100 g of FOS (n = 7 in the 6% FOS group and n = 8 in the other diet groups). After an adaptation period of 2 wk, rats were orally infected with 1.7 x 10(10) colony-forming units of S. enteritidis. Supplement-induced changes in the intestinal microflora and fecal cation excretion were determined before and after infection. Cytotoxicity of fecal water was determined with an in vitro bioassay, and fecal mucins were quantified fluorimetrically. Colonization of S. enteritidis was determined by quantification of salmonella in cecal contents and mucosa. Translocation of S. enteritidis was quantified by analysis of urinary nitric oxide metabolites in time. Before infection, FOS decreased cecal and fecal pH, increased fecal lactic acid concentration and increased bifidobacteria and enterobacteria. FOS also increased cytotoxicity of fecal water and fecal mucin excretion, indicating mucosal irritation. Remarkably, FOS dose-dependently increased salmonella numbers in cecal contents and mucosa and caused a major increase in infection-induced diarrhea. In addition, FOS enhanced translocation of salmonella. Thus, in contrast to most expectations, FOS dose-dependently impairs the resistance to salmonella infection in rats. These results await verification by other controlled animal and human studies.

摘要

益生元,如低聚果糖(FOS),可刺激具有保护作用的肠道微生物群,从而增加有机酸的产生。这可能会导致对酸敏感病原体的管腔杀灭增加。然而,宿主对侵袭性病原体(如沙门氏菌)的防御也取决于肠黏膜的屏障功能。益生元的快速发酵导致高浓度有机酸可能会损害屏障功能。因此,我们确定了日粮中FOS对大鼠抵抗肠炎沙门氏菌能力的剂量依赖性影响。给雄性Wistar大鼠喂食限量的“人源化”纯化日粮,分别添加0、3或6 g/100 g的FOS(6% FOS组n = 7,其他日粮组n = 8)。经过2周的适应期后,大鼠经口感染1.7×10¹⁰集落形成单位的肠炎沙门氏菌。在感染前后测定补充剂引起的肠道微生物群变化和粪便阳离子排泄。用体外生物测定法测定粪便水的细胞毒性,并用荧光法对粪便粘蛋白进行定量。通过对盲肠内容物和黏膜中的沙门氏菌进行定量来确定肠炎沙门氏菌的定植情况。通过及时分析尿中一氧化氮代谢产物来定量肠炎沙门氏菌的移位情况。在感染前,FOS降低了盲肠和粪便的pH值,增加了粪便乳酸浓度,并增加了双歧杆菌和肠杆菌。FOS还增加了粪便水的细胞毒性和粪便粘蛋白排泄,表明有黏膜刺激。值得注意的是,FOS剂量依赖性地增加了盲肠内容物和黏膜中的沙门氏菌数量,并导致感染引起的腹泻大幅增加。此外,FOS增强了沙门氏菌的移位。因此,与大多数预期相反,FOS剂量依赖性地损害了大鼠对沙门氏菌感染的抵抗力。这些结果有待其他对照动物和人体研究的验证。

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