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布拉氏酵母菌抑制组织炎症和细菌易位,作为其抵抗鼠伤寒沙门氏菌感染的保护机制之一。

Inhibition of tissue inflammation and bacterial translocation as one of the protective mechanisms of Saccharomyces boulardii against Salmonella infection in mice.

机构信息

Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.

出版信息

Microbes Infect. 2013 Apr;15(4):270-9. doi: 10.1016/j.micinf.2012.12.007. Epub 2013 Jan 30.

Abstract

Growing evidences suggest that Saccharomyces boulardii (SB) is efficacious against bacterial infections and inflammatory bowel diseases. This study investigated the effects of treatment with SB provided in a murine model of typhoid fever. Mice were divided into two groups: (1) control animals challenged with Salmonella Typhimurium (ST), and (2) animals receiving SB, and then challenged with ST. At days 0, 1, 5, 10 and 15 post-challenge, animals were euthanized and tissues collected to analyze bacterial translocation, cytokines, signaling pathways and histological analysis. Survival rate and animal weight were also evaluated. Treatment with SB increased survival rate and inhibited translocation of bacteria after ST challenge. Histological data showed that SB also protected mice against liver damage induced by ST. SB decreased levels of inflammatory cytokines and activation of mitogen-activated protein kinases (p38, JNK and ERK1/2), phospho-IκB, p65-RelA, phospho-jun and c-fos in the colon, signal pathways involved in the activation of inflammation induced by ST. Further experiments revealed that probiotic effects were due, at least in part, to the binding of ST to the yeast. Such binding diminishes ST translocation, resulting in decreased activation of signaling pathways which lead to intestinal inflammation in a murine model of typhoid fever.

摘要

越来越多的证据表明,布拉氏酵母菌(SB)对细菌感染和炎症性肠病有效。本研究在伤寒沙门氏菌感染的小鼠模型中研究了 SB 治疗的效果。将小鼠分为两组:(1)对照组,用鼠伤寒沙门氏菌(ST)攻击;(2)实验组,用 SB 预处理,然后用 ST 攻击。在攻毒后第 0、1、5、10 和 15 天,处死动物并收集组织,以分析细菌易位、细胞因子、信号通路和组织学分析。还评估了生存率和动物体重。用 SB 治疗可提高生存率并抑制 ST 攻击后的细菌易位。组织学数据表明,SB 还可防止 ST 引起的肝损伤。SB 降低了促炎细胞因子的水平,并抑制了 ST 诱导的丝裂原活化蛋白激酶(p38、JNK 和 ERK1/2)、磷酸化 IκB、p65-RelA、磷酸化 jun 和 c-fos 在结肠中的激活,这些信号通路参与了 ST 诱导的炎症激活。进一步的实验表明,益生菌的作用至少部分是由于 SB 与 ST 的结合。这种结合减少了 ST 的易位,从而减少了导致伤寒沙门氏菌感染的小鼠模型中肠道炎症的信号通路的激活。

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