...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Cag pathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection
【24h】

Cag pathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection

机译：胃上皮细胞对幽门螺杆菌感染的致病性岛特异性反应

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

Helicobacter pylori infects over half the world's population and causes a wide range of diseases, including gastritis, peptic ulcer, and two forms of gastric cancer. H. pylori infection elicits a variety of phenotypic responses in cultured gastric epithelial cells, including the expression of proinflammatory genes and changes in the actin cytoskeleton. Both of these responses are mediated by the type IV secretion system (TFSS) encoded by the cag pathogenicity island (cag PAI). We used human cDNA microarrays to examine the temporal transcriptional profiles of gastric AGS cells infected with H. pylori strain G27 and a panel of isogenic mutants to dissect the contributions of various genes in the cag PAI. Infection with G27 induced expression of genes involved in the innate immune response, cell shape regulation, and signal transduction. A mutant lacking the cagA gene, which encodes an effector molecule secreted by the TFSS and required for the host cell cytoskeletal response, induced the expression of fewer cytoskeletal genes. A mutant lacking cagE, which encodes a structural component of the TFSS, failed to up-regulate a superset of host genes, including the cagA-dependent genes, and many of the immune response genes. A mutant lacking the entire cag PAI failed to induce both the cagE-dependent genes and several transiently expressed cagE independent genes. Host cell transcriptional profiling of infection with isogenic strains offered a detailed molecular picture of H. pylori infection and provided insight into potential targets of individual virulence determinants such as tyrosine kinase and Rho GTPase signaling molecules.
机译：幽门螺杆菌感染了全球一半以上的人口，并引起多种疾病，包括胃炎，消化性溃疡和两种形式的胃癌。幽门螺杆菌感染在培养的胃上皮细胞中引起多种表型反应，包括促炎基因的表达和肌动蛋白细胞骨架的变化。这两种反应均由cag致病岛（cag PAI）编码的IV型分泌系统（TFSS）介导。我们使用人类cDNA微阵列检查了幽门螺杆菌G27感染的胃AGS细胞的时间转录谱和一组同基因突变体，以分析cag PAI中各种基因的贡献。 G27感染可诱导涉及先天免疫应答，细胞形状调节和信号转导的基因表达。缺少cagA基因的突变体，其编码由TFSS分泌的，是宿主细胞细胞骨架反应所必需的效应子分子，诱导了较少的细胞骨架基因的表达。缺少cagE的突变体，其编码TFSS的结构成分，未能上调宿主基因的超集，包括cagA依赖性基因和许多免疫应答基因。缺少整个cag PAI的突变体无法诱导cagE依赖性基因和几个瞬时表达的cagE非依赖性基因。用等基因菌株感染的宿主细胞转录谱提供了幽门螺杆菌感染的详细分子图片，并提供了对单个毒力决定因素（例如酪氨酸激酶和Rho GTPase信号分子）潜在目标的了解。

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