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首页> 外文学位 >Enterotoxigenic Escherichia coli promotes its adherence to intestinal epithelial cells through heat-labile enterotoxin-dependent and independent mechanisms.
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Enterotoxigenic Escherichia coli promotes its adherence to intestinal epithelial cells through heat-labile enterotoxin-dependent and independent mechanisms.

机译：产肠毒素的大肠杆菌通过不耐热的肠毒素依赖性和非依赖性机制来促进其对肠上皮细胞的粘附。

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摘要

Enterotoxigenic Escherichia coli (ETEC) is the most common etiology of travelers' diarrhea and a major endemic health threat in developing nations. While human infection with ETEC is relatively uncommon in industrialized countries, infection of pigs with host-specific porcine ETEC causes post-weaning diarrhea that is a significant burden to the pork industry. Despite the global prevalence and importance of these enteric pathogens, the full complement of virulence determinants responsible for intestinal colonization remains undetermined. Given recent evidence suggesting that the heat-labile enterotoxin (LT) provides a distinct colonization advantage for ETEC in vivo, we hypothesized that LT preconditions the host intestinal epithelium for ETEC adherence. To test this hypothesis, we used an in vitro model of ETEC adherence to examine more closely the role of LT in promoting bacterial-host interactions. Here we present data demonstrating that elaboration of LT promotes a significant increase in E. coli adherence. We also determined that increased adherence is dependent on the ADP-ribosylating activity of LT. Experiments are also presented that probe the ability of porcine ETEC isolates to induce apoptosis and cell death in porcine intestinal epithelial cells. Quantification of changes in host phosphatidylserine exposure following ETEC infection suggests that ETEC induce early stages of host apoptosis independent of LT. ETEC infection also causes a drastic inhibition of host esterase activity. We raise the possibility that ETEC may induce the early stages of host apoptosis to gain access to otherwise cryptic host receptors.
机译：产肠毒素的大肠杆菌（ETEC）是旅行者腹泻的最常见病因，也是发展中国家的主要地方性健康威胁。尽管在工业化国家中人感染ETEC的情况相对不常见，但宿主宿主猪ETEC感染猪后会导致断奶后腹泻，这对猪肉行业来说是沉重的负担。尽管这些肠道病原菌在全球范围内普遍存在并具有重要意义，但仍不确定致肠菌定植的致病因素的完整补充。鉴于最近的证据表明，热不稳定性肠毒素（LT）在体内为ETEC提供了独特的定殖优势，我们假设LT可以对宿主肠上皮进行ETEC粘附的预处理。为了检验该假设，我们使用了ETEC依从性的体外模型来更仔细地研究LT在促进细菌-宿主相互作用中的作用。在这里，我们提供的数据表明，精心设计的LT可以促进大肠杆菌依从性的显着提高。我们还确定增加的依从性取决于LT的ADP-核糖基化活性。还提出了实验，以探究猪ETEC分离物诱导猪肠道上皮细胞凋亡和细胞死亡的能力。量化ETEC感染后宿主磷脂酰丝氨酸暴露的变化，表明ETEC诱导了独立于LT的宿主凋亡的早期阶段。 ETEC感染还引起宿主酯酶活性的急剧抑制。我们提出了ETEC可能诱导宿主细胞凋亡的早期阶段，以获取其他方式隐秘的宿主受体的可能性。

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  • 作者

    Johnson, Amber M.;

  • 作者单位

    South Dakota State University.;

  • 授予单位 South Dakota State University.;
  • 学科 Biology Microbiology.;Biology Cell.
  • 学位 M.S.
  • 年度 2008
  • 页码 108 p.
  • 总页数 108
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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