首页> 外文学位 >Modulation of Escherichia coli O157:H7 mediated production of proinflammatory mediators by two species of Lactobacilli in two conditionally immortal colon epithelial cell lines.
【24h】

Modulation of Escherichia coli O157:H7 mediated production of proinflammatory mediators by two species of Lactobacilli in two conditionally immortal colon epithelial cell lines.

机译:大肠杆菌O157:H7对两种条件下永生的结肠上皮细胞系中两种乳酸杆菌的促炎介质产生的调节。

获取原文
获取原文并翻译 | 示例

摘要

We hypothesized that probiotic bacteria, Lactobacillus casei (LC) and Lactobacillus reuteri (LR) would decrease production of proinflammatory mediators (e.g. nitric oxide [NO], chemotactic cytokines [MIP-2, TNF-a by ELISA]) in response to exposure to bacterial pathogen E.coli O157:H7 (EC). Two non-tumorigenic murine colon epithelial cell lines (i.e. Young Adult Mouse Colon [YAMC, Apc+/+]; Immortomouse/Min Colon Epithelial [IMCE], ApcMin/+ cells) were used to assess the production of NO and cytokines when treated with bacteria, spent medium or both.;EC caused a concentration-dependent increase in NO and MIP-2 production compared to control (p 0.001). LC and LR co-treatment with EC caused a decrease (p 0.001) in NO production compared to EC treatment in both cell types. EC/LC co-treatment also attenuated (p 0.001) MIP-2 production compared to EC treatment.;The use of inhibitors of NF-kB, p38 MAPK, and JNK individually and p38 MAPK/JNK in combination accomplished partial inhibition (p 0.001) of EC induced NO and MIP-2 production. The use of hemoglobin indicated an NO-independent mechanism was activated in the presence of EC in potentiation of MIP-2 production. These results suggest that probiotic bacteria influence proinflammatory mediator production in colon-epithelial cells in a genus- and species- specific fashion, affecting both quantity of immune cells and type attracted under inflammatory conditions.
机译:我们假设益生菌,干酪乳杆菌(LC)和路氏乳杆菌(LR)会因暴露于暴露而降低促炎性介质(例如一氧化氮[NO],趋化性细胞因子[MIP-2,TNF-a ELISA])的产生细菌病原体大肠杆菌O157:H7(EC)。两种非致瘤鼠结肠上皮细胞系(即成年小鼠结肠[YAMC,Apc + / +]; Immunomouse / Min结肠上皮[IMCE],ApcMin / +细胞)被用于评估经NO处理的NO和细胞因子的产生。与对照相比,EC导致NO和MIP-2产生浓度依赖性增加(p <0.001)。在两种细胞类型中,与EC处理相比,LC和LR与EC共同处理导致NO生成减少(p <0.001)。与EC治疗相比,EC / LC联合治疗还减少了(p <0.001)MIP-2的产生;;单独使用NF-kB,p38 MAPK和JNK抑制剂以及将p38 MAPK / JNK联合使用可实现部分抑制(p <0.001)EC诱导NO和MIP-2的产生。血红蛋白的使用表明在EC的存在下,NO依赖性机制在MIP-2产生增强中被激活。这些结果表明,益生菌细菌以属和种特异性的方式影响结肠上皮细胞中促炎性介质的产生,从而影响免疫细胞的数量和在炎症条件下吸引的类型。

著录项

  • 作者

    Block, Erica M.;

  • 作者单位

    Michigan State University.;

  • 授予单位 Michigan State University.;
  • 学科 Health Sciences Nutrition.;Health Sciences Immunology.
  • 学位 M.S.
  • 年度 2004
  • 页码 117 p.
  • 总页数 117
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 预防医学、卫生学;预防医学、卫生学;
  • 关键词

  • 入库时间 2022-08-17 11:43:35

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号