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Induction of antibiotic tolerance in bacteria by self-produced and inter-species signaling.

机译：通过自生和种间信号传导诱导细菌对抗生素的耐受性。

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摘要

Though most bacteria within a population are killed by high concentrations of antibiotics, tolerant bacteria survive and can re-grow once antibiotics are removed. Bacterial persisters are dormant cells within an isogenic bacterial population that are tolerant to antibiotic treatment and have been implicated in chronic and recurrent infections. Tolerant and persistent bacteria are generated heterogeneously within populations, and a complete understanding of the processes by which these cells are formed remains elusive. However, there is increasing evidence that bacterial communication by chemical signaling plays a role in establishing population heterogeneity.;Here I show that bacterial communication induces persistence in Escherichia coli using the self-produced signaling molecule indole. lndole-induced persister formation was monitored using microfluidics, and oxidative stress and phage-shock pathways were determined to play a role in this phenomenon. I propose a model in which indole signaling "inoculates" a bacterial sub-population against antibiotics by activating stress responses, leading to persister formation.;Having demonstrated that communication using the signaling molecule indole controls persistence in the intestinal bacterium E. coli, I sought to determine whether indole could be used as an interspecies signal to control antibiotic tolerance in mixed microbial communities. The common bacterial pathogen Salmonella typhimurium was chosen for these experiments because this species, though closely related to E. coli, does not produce indole. The results demonstrated that indole signaling by E. coli induces tolerance to antibiotics in S. typhimurium. Further, the data suggest that indole-induced tolerance in S. typhimurium is mediated at least in part by the phage shock and oxidative stress response pathways, which were previously implicated in control of indole-induced persistence in E. coli. I used C. elegans as a simple in vivo model for gastrointestinal infection with S. typhimurium, demonstrating that indole signaling increased Salmonella tolerance and altered heterogeneity of infection in this system. These results suggest that antibiotic tolerance in pathogens may be induced by interception of bacterial signals in the host environment.
机译：尽管人群中的大多数细菌都被高浓度的抗生素杀死，但耐受的细菌可以生存，一旦去除抗生素，它们便可以重新生长。细菌残留物是同基因细菌种群中的休眠细胞，它们耐受抗生素治疗，并且与慢性和复发性感染有关。耐性细菌和持久性细菌在种群中异质地产生，并且对这些细胞形成过程的完整了解仍然难以捉摸。但是，越来越多的证据表明，通过化学信号传导进行的细菌传播在建立种群异质性中起着作用。在此，我证明了细菌传播利用自行产生的信号分子吲哚诱导了大肠杆菌的持久性。使用微流控技术监测吲哚诱导的持续性形成，并确定氧化应激和噬菌体途径在这种现象中起作用。我提出了一个模型，其中吲哚通过激活应激反应“诱导”细菌亚群对抗抗生素，从而导致持久性形成。;已经证明使用信号分子吲哚的通讯控制了肠道细菌大肠杆菌的持久性，我寻求确定是否可以将吲哚用作种间信号来控制混合微生物群落中的抗生素耐受性。这些实验选择了常见的细菌病原体鼠伤寒沙门氏菌，因为该物种尽管与大肠杆菌密切相关，但不会产生吲哚。结果表明大肠杆菌的吲哚信号传导诱导鼠伤寒沙门氏菌对抗生素的耐受。此外，数据表明，吲哚诱导的鼠伤寒沙门氏菌的耐受性至少部分地由噬菌体休克和氧化应激反应途径介导，它们先前与控制吲哚诱导的在大肠杆菌中的持久性有关。我使用秀丽隐杆线虫作为鼠伤寒沙门氏菌胃肠道感染的简单体内模型，证明了吲哚信号增强了沙门氏菌的耐受性并改变了该系统中感染的异质性。这些结果表明，宿主环境中细菌信号的拦截可能诱导了病原体对抗生素的耐受性。

著录项

  • 作者

    Vega, Nicole M.;

  • 作者单位

    Boston University.;

  • 授予单位 Boston University.;
  • 学科 Biology Molecular.;Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 157 p.
  • 总页数 157
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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