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首页> 外文学位 >Characterization of host-pathogen interaction of two bacterial toxins: Anthrax edema toxin and Escherichia coli cytolethal distending toxin.
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Characterization of host-pathogen interaction of two bacterial toxins: Anthrax edema toxin and Escherichia coli cytolethal distending toxin.

机译：两种细菌毒素：炭疽水肿毒素和大肠杆菌细胞致死性扩张毒素的宿主-病原体相互作用的表征。

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摘要

Pathogenic and symbiotic bacteria have developed mechanisms that promote survival and propagation within the host. In the case of symbiotic bacteria, the mechanisms developed are generally not harmful to the host. Pathogenic bacteria, however, have developed mechanisms that cause damage to the host thereby contributing to disease. These mechanisms include a broad range of virulence factors involved in such tasks as bacterial invasion, adhesion, internalization (in the case of intracellular pathogens), modulation of host cell functions, resisting/counteracting host immune defenses, and in some cases, activation of the immune system. In many instances, these virulence factors mimic host cell molecules and allow pathogens to hijack or modulate cellular functions. The expression of multiple virulence factors allow pathogens to exploit host cell functions and subvert host immune defenses for the ultimate survival of the bacteria. A full understanding on the mode of entry, action and effect on target host cells is required to fully comprehend disease progression triggered by a particular pathogen, as well as to provide better insight into disease treatment. In this work I present characterization of toxins produced by Bacillus anihracis and a family of toxins, termed cytolethal distending toxin (CDT), produced by various Gram negative bacteria. Chapters 2-4 present work addressing the mode of action and modulation of host cell response by edema toxin produced by B. anthraces. Chapter 5 presents work dealing with the host cell factors required for binding and entry of CDT produced by Escherichia coli (EcCDT).
机译：致病性和共生细菌已开发出促进宿主内存活和繁殖的机制。就共生细菌而言，所形成的机制通常对宿主无害。然而，致病细菌已发展出对宿主造成损害从而导致疾病的机制。这些机制包括广泛的毒力因子，例如细菌入侵，粘附，内在化（对于细胞内病原体而言），宿主细胞功能的调节，抵抗/抵消宿主免疫防御以及在某些情况下激活免疫系统。在许多情况下，这些毒力因子模拟宿主细胞分子并允许病原体劫持或调节细胞功能。多种毒力因子的表达使病原体能够利用宿主细胞的功能并破坏宿主的免疫防御力，从而使细菌最终存活。必须全面了解靶宿主细胞的进入方式，作用和作用，才能充分理解由特定病原体触发的疾病进展，并提供对疾病治疗的更好了解。在这项工作中，我介绍了由芽孢杆菌产生的毒素的特征以及由各种革兰氏阴性细菌产生的称为细胞致死性扩展毒素（CDT）的毒素家族。第2-4章介绍了炭疽杆菌产生的浮肿毒素对宿主细胞应答的作用方式和调节模式。第5章介绍了处理大肠杆菌（EcCDT）产生的CDT的结合和进入所需的宿主细胞因子。

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  • 作者

    Maldonado-Arocho, Francisco J.;

  • 作者单位

    University of California, Los Angeles.;

  • 授予单位 University of California, Los Angeles.;
  • 学科 Biology Molecular.;Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 237 p.
  • 总页数 237
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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