...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Enterohemorrhagic Escherichia coliO157:H7 Produces Tir, Which Is Translocated to the Host Cell Membrane but Is Not Tyrosine Phosphorylated
【24h】

Enterohemorrhagic Escherichia coliO157:H7 Produces Tir, Which Is Translocated to the Host Cell Membrane but Is Not Tyrosine Phosphorylated

机译：肠出血性大肠杆菌O157：H7产生Tir，该Tir易位至宿主细胞膜，但未酪氨酸磷酸化

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Intimate attachment to the host cell leading to the formation of attaching and effacing (A/E) lesions is an essential feature of enterohemorrhagic Escherichia coli (EHEC) O157:H7 pathogenesis. In a related pathogen, enteropathogenic E. coli (EPEC), this activity is dependent upon translocation of the intimin receptor, Tir, which becomes tyrosine phosphorylated within the host cell membrane. In contrast, the accumulation of tyrosine-phosphorylated proteins beneath adherent EHEC bacteria does not occur, leading to questions about whether EHEC uses a Tir-based mechanism for adherence and A/E lesion formation. In this report, we demonstrate that EHEC produces a functional Tir that is inserted into host cell membranes, where it serves as an intimin receptor. However, unlike in EPEC, in EHEC Tir is not tyrosine phosphorylated yet plays a key role in both bacterial adherence to epithelial cells and pedestal formation. EHEC, but not EPEC, was unable to synthesize Tir in Luria-Bertani medium but was able to secrete Tir into M9 medium, suggesting that Tir synthesis and secretion may be regulated differently in these two pathogens. EHEC Tir and EPEC Tir both bind intimin and focus cytoskeletal rearrangements, indicating that tyrosine phosphorylation is not needed for pedestal formation. EHEC and EPEC intimins are functionally interchangeable, but EHEC Tir shows a much greater affinity for EHEC intimin than for EPEC intimin. These findings highlight some of the differences and similarities between EHEC and EPEC virulence mechanisms, which can be exploited to further define the molecular basis of pedestal formation.
机译：紧密附着于宿主细胞导致附着和脱落（A / E）病变的形成是肠出血性大肠杆菌（EHEC）O157：H7发病机理的基本特征。在相关的病原体中，肠致病菌 E。大肠杆菌（EPEC），这种活性取决于内膜素受体Tir的转运，后者在宿主细胞膜内被酪氨酸磷酸化。相比之下，酪氨酸磷酸化蛋白在粘附的EHEC细菌下不会积累，从而引发了有关EHEC是否使用基于Tir的粘附和A / E病变形成机制的疑问。在此报告中，我们证明EHEC产生功能性Tir，该Tir插入宿主细胞膜，在其中充当内膜素受体。但是，与EPEC不同，在EHEC中，Tir并未被酪氨酸磷酸化，但在细菌对上皮细胞的粘附和基座形成中均起着关键作用。 EHEC，但不是EPEC，无法在Luria-Bertani培养基中合成Tir，但能够将Tir分泌到M9培养基中，这表明在这两种病原体中Tir的合成和分泌可能受到不同的调节。 EHEC Tir和EPEC Tir都结合内膜蛋白并聚焦细胞骨架重排，这表明不需要酪氨酸磷酸化来形成基座。 EHEC和EPEC内膜蛋白在功能上是可互换的，但是EHEC Tir对EHEC内膜蛋白的亲和力比对EPEC内膜蛋白的亲和力大得多。这些发现凸显了EHEC和EPEC毒力机制之间的某些差异和相似之处，可以用来进一步定义基座形成的分子基础。

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