当前位置: X-MOL 学术Annu. Rev. Microbiol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Autophagy Evasion and Endoplasmic Reticulum Subversion: The Yin and Yang of Legionella Intracellular Infection
Annual Review of Microbiology ( IF 10.5 ) Pub Date : 2016-09-08 00:00:00 , DOI: 10.1146/annurev-micro-102215-095557
Racquel Kim Sherwood 1 , Craig R. Roy 1
Affiliation  

The gram-negative bacterial pathogen Legionella pneumophila creates a novel organelle inside of eukaryotic host cells that supports intracellular replication. The L. pneumophila–containing vacuole evades fusion with lysosomes and interacts intimately with the host endoplasmic reticulum (ER). Although the natural hosts for L. pneumophila are free-living protozoa that reside in freshwater environments, the mechanisms that enable this pathogen to replicate intracellularly also function when mammalian macrophages phagocytose aerosolized bacteria, and infection of humans by L. pneumophila can result in a severe pneumonia called Legionnaires' disease. A bacterial type IVB secretion system called Dot/Icm is essential for intracellular replication of L. pneumophila. The Dot/Icm apparatus delivers over 300 different bacterial proteins into host cells during infection. These bacterial proteins have biochemical activities that target evolutionarily conserved host factors that control membrane transport processes, which results in the formation of the ER-derived vacuole that supports L. pneumophila replication. This review highlights research discoveries that have defined interactions between vacuoles containing L. pneumophila and the host ER. These studies reveal how L. pneumophila creates a vacuole that supports intracellular replication by subverting host proteins that control biogenesis and fusion of early secretory vesicles that exit the ER and host proteins that regulate the shape and dynamics of the ER. In addition to recruiting ER-derived membranes for biogenesis of the vacuole in which L. pneumophila replicates, these studies have revealed that this pathogen has a remarkable ability to interfere with the host's cellular process of autophagy, which is an ancient cell autonomous defense pathway that utilizes ER-derived membranes to target intracellular pathogens for destruction. Thus, this intracellular pathogen has evolved multiple mechanisms to control membrane transport processes that center on the involvement of the host ER.

中文翻译:

自噬逃避和内质网的颠覆:军团菌胞内感染的阴阳。

革兰氏阴性细菌病原体肺炎军团菌在真核宿主细胞内部产生了一种新型细胞器,该细胞器支持细胞内复制。在嗜肺军团菌的含液泡回避与溶酶体融合和相互作用紧密地与主机内质网(ER)。虽然自然宿主嗜肺军团菌是自由生活的原生动物驻留在淡水环境中,使这种病菌的机制在细胞内复制也功能时哺乳动物巨噬细胞吞噬细菌的雾化,并通过人类感染嗜肺军团菌会导致严重的肺炎,称为军团病。称为Dot / Icm的IVB型细菌分泌系统对于嗜肺乳杆菌的细胞内复制至关重要。在感染过程中,Dot / Icm设备将300多种不同的细菌蛋白输送到宿主细胞中。这些细菌蛋白具有针对进化保守的宿主因子的生化活性,这些宿主因子控制着膜的运输过程,从而导致了由ER衍生的液泡的形成,从而支持嗜肺乳杆菌的复制。这篇综述突出了已经确定了包含嗜肺乳杆菌的液泡和宿主ER之间相互作用的研究发现。这些研究揭示了嗜肺乳杆菌通过破坏宿主蛋白(控制退出ER的早期分泌囊泡的生物发生和融合)和调节ER形状和动力学的宿主蛋白,产生一种支持细胞内复制的液泡。这些研究表明,除了招募ER衍生的膜用于肺炎嗜血杆菌复制的液泡的生物发生外,这些研究还表明,这种病原体具有显着的能力来干扰宿主的自噬细胞过程,这是一种古老的细胞自主防御途径,利用ER衍生的膜靶向细胞内病原体进行破坏。因此,这种细胞内病原体已经进化出多种机制来控制以宿主ER的参与为中心的膜转运过程。
更新日期:2017-06-21
down
wechat
bug