• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Some structures and processes of human epithelial cells involved in uptake of enterohemorrhagic Escherichia coli O157:H7 strains.
【24h】

Some structures and processes of human epithelial cells involved in uptake of enterohemorrhagic Escherichia coli O157:H7 strains.

机译：人上皮细胞的一些结构和过程涉及肠出血性大肠杆菌O157：H7菌株的摄取。

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

摘要

Several enterohemorrhagic Escherichia coli (EHEC) strains of serotype O157:H7 isolated from patients with hemorrhagic colitis, ischemic colitis, or hemolytic uremic syndrome were all found to be able to invade certain human epithelial cell lines in vitro. Their ability to gain entry into epithelial cells was compared with those of known invasive Shigella flexneri and Salmonella typhi strains and the noninvasive E. coli strain HB101 in invasion assays utilizing gentamicin to kill extracellular bacteria. All EHEC strains under investigation were efficiently internalized into T24 bladder and HCT-8 ileocecal cells. In striking contrast to shigellae, the same EHEC strains were not taken up into human embryonic intestinal INT407 cells or HEp-2 cells any more than the noninvasive E. coli strain HB101. The mechanism(s) of EHEC internalization was characterized by comparing the invasion efficiencies in the absence and presence of a variety of inhibitors acting on structures and processes of prokaryotic or eukaryotic cells. Also, wild-type, plasmid-containing EHEC strains were compared with their plasmid-cured isogenic derivative strains to determine if plasmid genes affect invasion ability. Plasmid-cured EHEC invaded as well as wild-type EHEC, indicating that invasion ability is chromosomally encoded. Inhibition of bacterial protein synthesis by simultaneous addition of bacteria and chloramphenicol to the monolayer blocked EHEC uptake dramatically, suggesting the presence of an invasion protein(s) with a short half-life. Studies utilizing inhibitors which act on eukaryotic cells demonstrated a strong dependence on microfilaments in the process of uptake of all EHEC strains into both T24 and HCT-8 cells. In general, depolymerization of microtubules as well as inhibition of receptor-mediated endocytosis reduced the efficiency of EHEC invasion of T24 cells, whereas interference with endosome acidification reduced EHEC entry into only HCT-8 cells. Taxol-induced stabilization of microtubules did not inhibit internalization into T24 cells or into the HCT-8 cell line. In marked contrast, the ability of S. typhi Ty2 to invade either cell line was inhibited only by depolymerization of microfilaments. In addition to the cell line specificity of EHEC invasion, not all EHEC strains displayed uniform behavior in the presence of inhibitors, suggesting the existence of variant uptake pathways in different strains. Most importantly, previous reports of the inability of EHEC to invade INT407 or HEp-2 cell lines support the currently held belief that EHEC strains are noninvasive.(ABSTRACT TRUNCATED AT 400 WORDS)
机译：从出血性结肠炎，缺血性结肠炎或溶血性尿毒症综合征患者中分离出的几种O157：H7血清型肠出血性大肠杆菌（EHEC）菌株均可在体外侵袭某些人上皮细胞系。在利用庆大霉素杀死细胞外细菌的侵袭试验中，将它们进入上皮细胞的能力与已知的侵袭性志贺氏菌和鼠伤寒沙门氏菌菌株以及非侵害性大肠杆菌HB101菌株进行了比较。所有正在研究的EHEC菌株均有效地内化到T24膀胱和HCT-8回盲细胞中。与志贺氏菌形成鲜明对比的是，与无创性大肠杆菌HB101相比，相同的EHEC菌株没有被吸收到人胚肠道INT407细胞或HEp-2细胞中。 EHEC内在化的机制是通过比较在不存在和存在于原核或真核细胞的结构和过程中的各种抑制剂的情况下的侵入效率来表征的。同样，将野生型的含质粒的EHEC菌株与其质粒固化的同基因衍生物菌株进行比较，以确定质粒基因是否影响侵袭能力。质粒固化的EHEC以及野生型EHEC均被侵袭，表明入侵能力是通过染色体编码的。通过同时向单层添加细菌和氯霉素来抑制细菌蛋白质的合成，可显着阻止EHEC的摄取，表明存在半衰期短的入侵蛋白质。利用作用于真核细胞的抑制剂进行的研究表明，在将所有EHEC菌株吸收到T24和HCT-8细胞中的过程中，它们对微丝的依赖性很高。通常，微管解聚以及抑制受体介导的内吞作用降低了EHEC侵袭T24细胞的效率，而干扰内体酸化作用则降低了EHEC仅进入HCT-8细胞的进入。紫杉醇诱导的微管稳定作用不会抑制内化进入T24细胞或HCT-8细胞系。形成鲜明对比的是，伤寒沙门氏菌Ty2侵入任一细胞系的能力仅通过微丝的解聚得到抑制。除了EHEC入侵的细胞系特异性外，并非所有EHEC菌株在存在抑制剂的情况下均表现出一致的行为，这表明不同菌株中存在变异的摄取途径。最重要的是，以前关于EHEC无法入侵INT407或HEp-2细胞系的报道支持了目前认为EHEC菌株是非侵入性的观点（摘要截短了400字）。

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