...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The FEBS journal >Invasion of enteropathogenic Escherichia coli into host cells through epithelial tight junctions
【24h】

Invasion of enteropathogenic Escherichia coli into host cells through epithelial tight junctions

机译：肠致病性大肠杆菌通过上皮紧密连接侵入宿主细胞

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Enteropathogenic Escherichia coli (EPEC) has been shown to disrupt the barrier function of host intestinal epithelial tissues through entering tight junctions. However, the mechanism by which this occurs remains poorly understood. In this study, we determined that EPEC invades host cells through tight junctions as it initiates infection. Immunofluorescence microscopy revealed redistribution of the tight-junction proteins occludin and ZO-1 from an intercellular to a cytoplasmic location after EPEC invasion. Flotillin-1 was recruited to sites of EPEC entry. EPEC entered host cells through tight-junction membrane microdomains. Tight-junction ultrastructure was disrupted following EPEC infection, accompanied by loss of barrier function. EPEC infection caused a time-dependent decrease in trans-epithelial electrical resistance. Subcellular fractionation using discontinuous sucrose density gradients demonstrated a decline in raft-associated occludin following exposure to EPEC. These results indicate the important role of host membrane tight-junction microdomains in EPEC invasion.
机译：肠致病性大肠杆菌（EPEC）已显示通过进入紧密连接而破坏宿主肠上皮组织的屏障功能。但是，发生这种情况的机制仍然知之甚少。在这项研究中，我们确定了EPEC在引发感染时会通过紧密连接侵入宿主细胞。免疫荧光显微镜显示紧密连接蛋白occludin和ZO-1在EPEC入侵后从细胞间位置重新分布到细胞质位置。 Flotillin-1被募集到EPEC进入地点。 EPEC通过紧密连接的膜微区进入宿主细胞。 EPEC感染后，紧密连接的超微结构被破坏，并伴随屏障功能的丧失。 EPEC感染导致跨上皮电阻的时间依赖性下降。使用不连续蔗糖密度梯度的亚细胞分级分离显示，暴露于EPEC后，与筏相关的封闭素减少。这些结果表明宿主膜紧密连接微区在EPEC入侵中的重要作用。

著录项

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