Institute of Medical Microbiology, Department of Medicine, University of Zürich, Gloriastrasse 30/32, 8006 Zürich, Switzerland.
Max von Pettenkofer Institute, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9a, 80336 Munich, Germany.
Trends Microbiol. 2016 Jun;24(6):450-462. doi: 10.1016/j.tim.2016.02.003. Epub 2016 Feb 26.
Intracellular bacterial pathogens subvert the endocytic bactericidal pathway to form specific replication-permissive compartments termed pathogen vacuoles or inclusions. To this end, the pathogens employ type III or type IV secretion systems, which translocate dozens, if not hundreds, of different effector proteins into their host cells, where they manipulate vesicle trafficking and signaling pathways in favor of the intruders. While the distinct cocktail of effectors defines the specific processes by which a pathogen vacuole is formed, the different pathogens commonly target certain vesicle trafficking routes, including the endocytic or secretory pathway. Recently, the retrograde transport pathway from endosomal compartments to the trans-Golgi network emerged as an important route affecting pathogen vacuole formation. Here, we review current insight into the host cell's retrograde trafficking pathway and how vacuolar pathogens of the genera Legionella, Coxiella, Salmonella, Chlamydia, and Simkania employ mechanistically distinct strategies to subvert this pathway, thus promoting intracellular survival and replication.
细胞内细菌病原体颠覆内吞杀菌途径，形成称为病原体空泡或包含体的特定复制允许隔室。为此，病原体利用 III 型或 IV 型分泌系统，将数十种（如果不是数百种）不同的效应蛋白易位到宿主细胞中，在宿主细胞中，它们操纵囊泡运输和信号通路以有利于入侵者。虽然不同的效应物组合定义了形成病原体空泡的特定过程，但不同的病原体通常靶向某些囊泡运输途径，包括内吞或分泌途径。最近，从内体隔室到反式高尔基网络的逆行运输途径成为影响病原体空泡形成的重要途径。在这里，我们回顾宿主细胞逆行运输途径的最新见解，以及军团菌属、柯克斯体属、沙门氏菌属、衣原体属和 Simkania 属的囊泡病原体如何利用机制上不同的策略来颠覆这种途径，从而促进细胞内存活和复制。
