Mostowy Serge, Cossart Pascale
Institut Pasteur, Département de Biologie Cellulaire et Infection, Unité des Interactions Bactéries-Cellules, Paris, F-75015 France.
Cell Motil Cytoskeleton. 2009 Oct;66(10):816-23. doi: 10.1002/cm.20353.
The study of an infection process can reveal how microbes exploit the host, and can illuminate unknown host cellular functions. Invasive pathogens have evolved efficient strategies to promote their internalization within normally non-phagocytic host cells. The so-called "zippering" bacteria present to host cell receptors molecules that mimic endogenous ligands, thereby inducing specific intracellular signaling cascades ultimately resulting in actin polymerization and uptake. Here we review how the bacterial pathogen Listeria monocytogenes enters into cells, and present a series of studies revealing that in addition to actin rearrangements this bacterium exploits the clathrin-mediated endocytosis machinery together with septins, a novel cytoskeleton element. The challenge is now to decipher how all of these components orchestrate themselves to permit entry into normally non-phagocytic cells.
对感染过程的研究可以揭示微生物如何利用宿主，并能阐明未知的宿主细胞功能。侵袭性病原体已经进化出有效的策略来促进它们在正常非吞噬性宿主细胞内的内化。所谓的“拉链式”细菌向宿主细胞受体呈现模仿内源性配体的分子，从而诱导特定的细胞内信号级联反应，最终导致肌动蛋白聚合和摄取。在这里，我们综述了细菌病原体单核细胞增生李斯特菌如何进入细胞，并介绍了一系列研究，这些研究表明，除了肌动蛋白重排外，这种细菌还利用网格蛋白介导的内吞机制以及一种新型细胞骨架成分——隔膜蛋白。现在面临的挑战是解读所有这些成分如何协同作用，以允许进入正常的非吞噬细胞。
