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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inhibition of pathogen-induced apoptosis by a Coxiella burnetii type IV effector protein
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Inhibition of pathogen-induced apoptosis by a Coxiella burnetii type IV effector protein

机译：柯氏杆菌IV型效应蛋白抑制病原体诱导的细胞凋亡

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摘要

Coxiella burnetii and Legionella pneumophila are evolutionarily re lated pathogens with different intracellular infection strategies. C. burnetii persists within and is transmitted by mammalian hosts, whereas, L. pneumophila is found primarily in the environment associated with protozoan hosts. Although a type IV secretion sys tem encoded by the defect in organelle trafficking (dot) and intra cellular multiplication (icm) genes is a virulence determinant that remains highly conserved in both bacteria, the two pathogens en code a different array of effector proteins that are delivered into host cells by the Dot/lcm machinery. This difference suggests that adaptations to evolutionarily distinct hosts may be reflected in the effector protein repertoires displayed by these two pathogens. Here we provide evidence in support of this hypothesis. We show that a unique C. burnetii effector from the ankyrin repeat (Ank) family called AnkG interferes with the mammalian apoptosis path way. AnkG was found to interact with the host protein gC1qR (p32). Either the addition of AnkG to the repertoire of L. pneumo phila effector proteins or the silencing of p32 in mouse dendritic cells resulted in a gain of function that allowed intracellular repli cation of L. pneumophila in these normally restrictive mammalian host cells by preventing rapid pathogen-induced apoptosis. These data indicate that p32 regulates pathogen-induced apoptosis and that AnkG functions to block this pathway. Thus, emergence of an effector protein that interferes with a proapoptotic signaling path way directed against intracellular bacteria correlates with adap tation of a pathogen to mammalian hosts.
机译：伯氏柯氏杆菌和嗜肺军团菌是具有不同细胞内感染策略的进化相关病原体。伯氏梭菌仍存在于哺乳动物宿主中并由其传播，而肺炎衣原体主要存在于与原生动物宿主相关的环境中。尽管由细胞器运输（点）和细胞内增殖（icm）基因中的缺陷编码的IV型分泌系统是在两种细菌中均高度保守的毒力决定因素，但两种病原体编码的另一种效应蛋白通过Dot / lcm机械传递到宿主细胞中。这种差异表明，对进化上不同的宿主的适应性可能反映在这两种病原体展示的效应蛋白库中。在这里，我们提供了支持该假设的证据。我们表明，从锚蛋白重复（Ank）家族称为AnkG的独特的伯氏梭菌效应子干扰了哺乳动物细胞凋亡的途径。发现AnkG与宿主蛋白gC1qR（p32）相互作用。在鼠肺炎埃博拉氏菌效应蛋白库中添加AnkG或使小鼠树突状细胞中的p32沉默，都会导致功能增强，从而通过阻止快速致病菌在这些通常限制性的哺乳动物宿主细胞中实现肺炎链球菌的细胞内复制诱导的细胞凋亡。这些数据表明p32调节病原体诱导的细胞凋亡，而AnkG的功能是阻断该途径。因此，干扰针对细胞内细菌的促凋亡信号传导途径的效应蛋白的出现与病原体向哺乳动物宿主的适应有关。

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    Anja Luehrmann; Catarina V. Nogueira; Kimberly L. Carey; Craig R. Roy;

  • 作者单位

    Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536 Microbiology Institute, University Clinic Erlangen, FriedrichAlexander University of Erlangen-Nuremberg, 91054 Erlangen, Germany;

    rnSection of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536 Graduate Program in Areas of Basic and Applied Biology, Instituto de Ciencias Biomedicas Dr. Abel Salazar, Universidade do Porto, 4099-003 Porto, Portugal;

    rnSection of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536;

    rnSection of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    legionella pneumophila; ankyrin repeat proteins; gC1qR (p32); type IV secretion; pyroptosis;

    机译：嗜肺军团菌锚蛋白重复蛋白;gC1qR（p32）;IV型分泌物;发烧;

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