The recycling endosome and bacterial pathogens.

The recycling endosome and bacterial pathogens.
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DOI:
10.1111/cmi.12857
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发表时间:
2018-07
影响因子:
3.4
通讯作者:
Neunuebel MR
Neunuebel MR
中科院分区:
生物学2区
文献类型:
--
作者:
Allgood SC;Neunuebel MR

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细菌病原体已经发展了广泛的策略来在人类细胞内生存。许多病原体在液泡区室中繁殖,而其他病原体则可以破坏液泡并在宿主细胞质中复制。许多细菌病原体的共同主题是使用专门的分泌系统将效应蛋白递送到宿主细胞中。这些效应器可以操纵宿主的膜运输途径,将液泡重塑为允许复制的生态位并防止降解。作为真核生物膜运输的主要调节因子,Rab GTP酶是细菌效应子的主要靶点。这篇综述强调了几种细菌病原体,包括肺炎衣原体,沙眼衣原体,福氏志贺菌,沙门氏菌,肠道血清型鼠伤寒,尿路致病性大肠杆菌,嗜肺军团菌的Rab GTPases调节宿主循环内吞的操作。循环内吞作用在细胞的营养摄取、免疫、细胞分裂、迁移和粘附等方面起着关键作用。尽管关于利用Rab GTP酶的细菌病原体的分子基础和生物学相关性仍有许多有待理解,但目前的知识支持内吞再循环Rab GTP酶被差异靶向以避免降解并支持细菌复制的观点。因此,细菌病原体和宿主内吞再循环途径之间的相互作用的未来研究有望加深我们对细菌生存策略的理解。
Bacterial pathogens have developed a wide range of strategies to survive within human cells. A number of pathogens multiply in a vacuolar compartment, while others can rupture the vacuole and replicate in the host cytosol. A common theme among many bacterial pathogens is the use of specialized secretion systems to deliver effector proteins into the host cell. These effectors can manipulate the host’s membrane trafficking pathways to remodel the vacuole into a replication-permissive niche and prevent degradation. As master regulators of eukaryotic membrane traffic, Rab GTPases are principal targets of bacterial effectors. This review highlights the manipulation of Rab GTPases that regulate host recycling endocytosis by several bacterial pathogens including Chlamydia pneumoniae, Chlamydia trachomatis, Shigella flexneri, Salmonella enterica serovar Typhimurium, Uropathogenic Escherichia coli, and Legionella pneumophila. Recycling endocytosis plays key roles in a variety of cellular aspects such as nutrient uptake, immunity, cell division, migration and adhesion. Though much remains to be understood about the molecular basis and the biological relevance of bacterial pathogens exploiting Rab GTPases, current knowledge supports the notion that endocytic recycling Rab GTPases are differentially targeted to avoid degradation and support bacterial replication. Thus, future studies of the interactions between bacterial pathogens and host endocytic recycling pathways are poised to deepen our understanding of bacterial survival strategies.
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