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细菌病原体对宿主胞吐复合物的利用。

Exploitation of the host exocyst complex by bacterial pathogens.

机构信息

Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.

Department of Pathology, University of Otago, Dunedin, New Zealand.

出版信息

Mol Microbiol. 2023 Jul;120(1):32-44. doi: 10.1111/mmi.15034. Epub 2023 Feb 11.

DOI:10.1111/mmi.15034
PMID:36717381
Abstract

Intracellular bacterial pathogens remodel the plasma membrane of eukaryotic cells in order to establish infection. A common and well-studied mechanism of plasma membrane remodelling involves bacterial stimulation of polymerization of the host actin cytoskeleton. Here, we discuss recent results showing that several bacterial pathogens also exploit the host vesicular trafficking pathway of 'polarized exocytosis' to expand and reshape specific regions in the plasma membrane during infection. Polarized exocytosis is mediated by an evolutionarily conserved octameric protein complex termed the exocyst. We describe examples in which the bacteria Listeria monocytogenes, Salmonella enterica serovar Typhimurium, and Shigella flexneri co-opt the exocyst to promote internalization into human cells or intercellular spread within host tissues. We also discuss results showing that Legionella pneumophila or S. flexneri manipulate exocyst components to modify membrane vacuoles to favour intracellular replication or motility of bacteria. Finally, we propose potential ways that pathogens manipulate exocyst function, discuss how polarized exocytosis might promote infection and highlight the importance of future studies to determine how actin polymerization and polarized exocytosis are coordinated to achieve optimal bacterial infection.

摘要

细胞内细菌病原体重塑真核细胞的质膜以建立感染。质膜重塑的一个常见且研究充分的机制涉及细菌刺激宿主肌动蛋白细胞骨架的聚合。在这里,我们讨论了最近的结果,表明几种细菌病原体还利用宿主囊泡运输途径的“极化胞吐作用”在感染过程中扩展和重塑质膜的特定区域。极化胞吐作用是由一个被称为外泌体的进化上保守的八聚体蛋白复合物介导的。我们描述了细菌李斯特菌、沙门氏菌 Typhimurium 和志贺氏菌利用外泌体促进内化进入人细胞或在宿主组织内的细胞间传播的例子。我们还讨论了结果表明,嗜肺军团菌或志贺氏菌操纵外泌体成分来修饰膜囊泡,以有利于细菌的细胞内复制或运动。最后,我们提出了病原体操纵外泌体功能的潜在方式,讨论了极化胞吐作用如何促进感染,并强调了未来研究确定肌动蛋白聚合和极化胞吐作用如何协调以实现最佳细菌感染的重要性。

相似文献

1
Exploitation of the host exocyst complex by bacterial pathogens.细菌病原体对宿主胞吐复合物的利用。
Mol Microbiol. 2023 Jul;120(1):32-44. doi: 10.1111/mmi.15034. Epub 2023 Feb 11.
2
exploits host exocytosis to promote cell-to-cell spread.利用宿主胞吐作用促进细胞间传播。
Proc Natl Acad Sci U S A. 2020 Feb 18;117(7):3789-3796. doi: 10.1073/pnas.1916676117. Epub 2020 Feb 3.
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Shigella flexneri subverts host polarized exocytosis to enhance cell-to-cell spread.福氏志贺菌颠覆宿主极化胞吐作用以增强细胞间传播。
Mol Microbiol. 2021 Nov;116(5):1328-1346. doi: 10.1111/mmi.14827. Epub 2021 Oct 21.
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The Host Scaffolding Protein Filamin A and the Exocyst Complex Control Exocytosis during InlB-Mediated Entry of .宿主骨架蛋白细丝蛋白 A 和胞吐复合物在外膜囊泡复合物在 InlB 介导的入侵过程中控制胞吐作用。
Infect Immun. 2018 Dec 19;87(1). doi: 10.1128/IAI.00689-18. Print 2019 Jan.
5
Listeria monocytogenes Co-Opts the Host Exocyst Complex To Promote Internalin A-Mediated Entry.李斯特菌利用宿主胞吐复合物促进内毒素 A 介导入侵。
Infect Immun. 2022 Dec 15;90(12):e0032622. doi: 10.1128/iai.00326-22. Epub 2022 Oct 18.
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Listeria monocytogenes membrane trafficking and lifestyle: the exception or the rule?李斯特菌属膜运输和生活方式:例外还是规律?
Annu Rev Cell Dev Biol. 2009;25:649-70. doi: 10.1146/annurev.cellbio.042308.113331.
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The Host GTPase Arf1 and Its Effectors AP1 and PICK1 Stimulate Actin Polymerization and Exocytosis To Promote Entry of Listeria monocytogenes.宿主 GTPase Arf1 及其效应物 AP1 和 PICK1 刺激肌动蛋白聚合和胞吐作用,促进李斯特菌进入。
Infect Immun. 2020 Jan 22;88(2). doi: 10.1128/IAI.00578-19.
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A glance at Listeria and Salmonella cell invasion: different strategies to promote host actin polymerization.一眼看穿李斯特菌和沙门氏菌的细胞入侵:促进宿主肌动蛋白聚合的不同策略。
Int J Med Microbiol. 2012 Jan;302(1):19-32. doi: 10.1016/j.ijmm.2011.05.003. Epub 2011 Jul 23.
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Interaction of microbial pathogens with host exocytic pathways.微生物病原体与宿主胞吐途径的相互作用。
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Localization of alpha-actinin-4 during infections by actin remodeling bacteria.α-辅肌动蛋白-4在肌动蛋白重塑菌感染过程中的定位。
Anat Rec (Hoboken). 2021 Jul;304(7):1400-1419. doi: 10.1002/ar.24548. Epub 2020 Nov 5.

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