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2
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本文引用的文献

1
The Francisella tularensis pathogenicity island protein IglC and its regulator MglA are essential for modulating phagosome biogenesis and subsequent bacterial escape into the cytoplasm.土拉弗朗西斯菌致病岛蛋白IglC及其调节因子MglA对于调节吞噬体生物发生以及随后细菌逃逸到细胞质中至关重要。
Cell Microbiol. 2005 Jul;7(7):969-79. doi: 10.1111/j.1462-5822.2005.00526.x.
2
Modulation of biogenesis of the Francisella tularensis subsp. novicida-containing phagosome in quiescent human macrophages and its maturation into a phagolysosome upon activation by IFN-gamma.土拉弗朗西斯菌新凶手亚种含吞噬体在静止人巨噬细胞中的生物合成调控及其在γ干扰素激活后成熟为吞噬溶酶体的过程。
Cell Microbiol. 2005 Jul;7(7):957-67. doi: 10.1111/j.1462-5822.2005.00529.x.
3
Maturation of the Legionella pneumophila-containing phagosome into a phagolysosome within gamma interferon-activated macrophages.嗜肺军团菌吞噬体在γ干扰素激活的巨噬细胞内成熟为吞噬溶酶体。
Infect Immun. 2005 May;73(5):3166-71. doi: 10.1128/IAI.73.5.3166-3171.2005.
4
Amoebae as training grounds for intracellular bacterial pathogens.变形虫作为细胞内细菌病原体的训练场。
Appl Environ Microbiol. 2005 Jan;71(1):20-8. doi: 10.1128/AEM.71.1.20-28.2005.
5
Differentiate to thrive: lessons from the Legionella pneumophila life cycle.分化以求生存:嗜肺军团菌生命周期的启示
Mol Microbiol. 2004 Jul;53(1):29-40. doi: 10.1111/j.1365-2958.2004.04129.x.
6
Disruption of the phagosomal membrane and egress of Legionella pneumophila into the cytoplasm during the last stages of intracellular infection of macrophages and Acanthamoeba polyphaga.在巨噬细胞和多噬棘阿米巴细胞内感染的最后阶段,嗜肺军团菌的吞噬体膜破裂并逸出到细胞质中。
Infect Immun. 2004 Jul;72(7):4040-51. doi: 10.1128/IAI.72.7.4040-4051.2004.
7
The LetE protein enhances expression of multiple LetA/LetS-dependent transmission traits by Legionella pneumophila.LetE蛋白增强了嗜肺军团菌多种LetA/LetS依赖性传播特性的表达。
Infect Immun. 2004 Jun;72(6):3284-93. doi: 10.1128/IAI.72.6.3284-3293.2004.
8
Cell biology of the intracellular infection by Legionella pneumophila.嗜肺军团菌细胞内感染的细胞生物学
Microbes Infect. 2004 Jan;6(1):129-39. doi: 10.1016/j.micinf.2003.11.004.
9
Activation of caspase-3 by the Dot/Icm virulence system is essential for arrested biogenesis of the Legionella-containing phagosome.Dot/Icm 毒力系统对caspase-3的激活对于含军团菌吞噬体生物合成的停滞至关重要。
Cell Microbiol. 2004 Jan;6(1):33-48. doi: 10.1046/j.1462-5822.2003.00335.x.
10
Macroautophagy is dispensable for intracellular replication of Legionella pneumophila in Dictyostelium discoideum.巨自噬对于嗜肺军团菌在盘基网柄菌中的细胞内复制并非必需。
Mol Microbiol. 2004 Jan;51(1):63-72. doi: 10.1046/j.1365-2958.2003.03826.x.

嗜肺军团菌的RpoS而非RelA在调节吞噬体生物发生及适应吞噬体微环境中的作用。

Role for RpoS but not RelA of Legionella pneumophila in modulation of phagosome biogenesis and adaptation to the phagosomal microenvironment.

作者信息

Abu-Zant Alaeddin, Asare Rexford, Graham James E, Abu Kwaik Yousef

机构信息

Department of Microbiology, University of Louisville College of Medicine, Louisville, KY 40292, USA.

出版信息

Infect Immun. 2006 May;74(5):3021-6. doi: 10.1128/IAI.74.5.3021-3026.2006.

DOI:10.1128/IAI.74.5.3021-3026.2006
PMID:16622243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1459718/
Abstract

The induction of virulence traits by Legionella pneumophila at the post-exponential phase has been proposed to be triggered by the stringent response mediated by RelA, which triggers RpoS. We show that L. pneumophila rpoS but not relA is required for early intracellular survival and replication within human monocyte-derived macrophages and Acanthamoeba polyphaga. In addition, L. pneumophila rpoS but not relA is required for expression of the pore-forming activity. We provide evidence that RpoS plays a role in the modulation of phagosome biogenesis and in adaptation to the phagosomal microenvironment. Thus, there is no functional link between the stringent response and RpoS in the pathogenesis of L. pneumophila.

摘要

嗜肺军团菌在指数生长后期诱导毒力特性被认为是由RelA介导的严谨反应触发的,RelA会触发RpoS。我们发现,嗜肺军团菌的RpoS而非RelA是其在人单核细胞衍生巨噬细胞和多噬棘阿米巴中早期细胞内存活和复制所必需的。此外,嗜肺军团菌的RpoS而非RelA是形成孔道活性表达所必需的。我们提供的证据表明,RpoS在吞噬体生物发生的调节以及对吞噬体微环境的适应中发挥作用。因此,在嗜肺军团菌的发病机制中,严谨反应与RpoS之间不存在功能联系。