...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Lon Protease Activity Causes Down-Regulation of Salmonella Pathogenicity Island 1 Invasion Gene Expression after Infection of Epithelial Cells
【24h】

Lon Protease Activity Causes Down-Regulation of Salmonella Pathogenicity Island 1 Invasion Gene Expression after Infection of Epithelial Cells

机译：Lon蛋白酶活性导致上皮细胞感染后沙门氏菌致病岛1入侵基因表达的下调。

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

摘要

Salmonella enterica serovar Typhimurium causes self-limiting gastroenteritis in humans and a typhoid-like disease in mice that serves as a model for typhoid infections in humans. A critical step in Salmonella pathogenesis is the invasion of enterocytes and M cells of the small intestine via expression of a type III secretion system, encoded on Salmonella pathogenicity island 1 (SPI-1), that secretes effector proteins into host cells, leading to engulfment of the bacteria within large membrane ruffles. The in vitro regulation of invasion genes has been the subject of much scientific investigation. Transcription of the hilA gene, which encodes an OmpR/ToxR-type transcriptional activator of downstream invasion genes, is increased during growth under high-osmolarity and low-oxygen conditions, which presumably mimic the environment found within the small intestine. Several negative regulators of invasion gene expression have been identified, including HilE, Hha, and Lon protease. Mutations within the respective genes increase the expression of hilA when the bacteria are grown under environmental conditions that are not favorable for hilA expression and invasion. In this study, the intracellular expression of invasion genes was examined, after bacterial invasion of HEp-2 epithelial cells, using Salmonella strains containing plasmid-encoded short-half-life green fluorescent protein reporters of hilA, hilD, hilC, or sicA expression. Interestingly, the expression of SPI-1 genes was down-regulated after invasion, and this was important for the intracellular survival of the bacteria. In addition, the effects of mutations in genes encoding negative regulators of invasion on intracellular hilA expression were examined. Our results indicate that Lon protease is important for down-regulation of hilA expression and intracellular survival after the invasion of epithelial cells.
机译：鼠伤寒沙门氏菌引起人类自限性肠胃炎，小鼠伤寒样疾病可作为人类伤寒感染的模型。沙门氏菌发病机理中的关键步骤是通过表达在沙门氏菌致病岛1（SPI-）上的III型分泌系统的表达，侵袭小肠的肠细胞和M细胞。 1），将效应蛋白分泌到宿主细胞中，导致细菌吞入大的膜褶中。入侵基因的体外调控已成为许多科学研究的主题。在高渗透压和低氧条件下，在生长过程中，增加了 hilA 基因的转录，该基因编码下游入侵基因的OmpR / ToxR型转录激活因子，大概是模拟了该环境中的环境。小肠。已经鉴定出几种入侵基因表达的负调节剂，包括HilE，Hha和Lon蛋白酶。当细菌在不利于 hilA 表达和入侵的环境条件下生长时，各个基因内的突变会增加 hilA 的表达。在这项研究中，使用包含质粒编码的的半衰期绿色荧光蛋白报告基因的沙门氏菌菌株，检测了HEp-2上皮细胞被细菌入侵后入侵基因的细胞内表达。 hilA ， hilD ， hilC 或 sicA 表达式。有趣的是，SPI-1基因的表达在入侵后被下调，这对于细菌的细胞内存活很重要。另外，检查了编码侵袭负调节剂的基因中的突变对细胞内 hilA 表达的影响。我们的结果表明，Lon蛋白酶对于上皮细胞侵袭后下调 hilA 表达和细胞内存活很重要。

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