Tilney L G, Portnoy D A
Department of Biology, University of Pennsylvania, Philadelphia 19104-6018.
J Cell Biol. 1989 Oct;109(4 Pt 1):1597-608. doi: 10.1083/jcb.109.4.1597.
Listeria monocytogenes was used as a model intracellular parasite to study stages in the entry, growth, movement, and spread of bacteria in a macrophage cell line. The first step in infection is phagocytosis of the Listeria, followed by the dissolution of the membrane surrounding the phagosome presumably mediated by hemolysin secreted by Listeria as nonhemolytic mutants remain in intact vacuoles. Within 2 h after infection, each now cytoplasmic Listeria becomes encapsulated by actin filaments, identified as such by decoration of the actin filaments with subfragment 1 of myosin. These filaments are very short. The Listeria grow and divide and the actin filaments rearrange to form a long tail (often 5 microns in length) extending from only one end of the bacterium, a "comet's tail," in which the actin filaments appear randomly oriented. The Listeria "comet" moves to the cell surface with its tail oriented towards the cell center and becomes incorporated into a cell extension with the Listeria at the tip of the process and its tail trailing into the cytoplasm behind it. This extension contacts a neighboring macrophage that phagocytoses the extension of the first macrophage. Thus, within the cytoplasm of the second macrophage is a Listeria with its actin tail surrounded by a membrane that in turn is surrounded by the phagosome membrane of the new host. Both these membranes are then solubilized by the Listeria and the cycle is repeated. Thus, once inside a host cell, the infecting Listeria and their progeny can spread from cell to cell by remaining intracellular and thus bypass the humoral immune system of the organism. To establish if actin filaments are essential for the spread of Listeria from cell to cell, we treated infected macrophages with cytochalasin D. The Listeria not only failed to spread, but most were found deep within the cytoplasm, rather than near the periphery of the cell. Thin sections revealed that the net of actin filaments is not formed nor is a "comet" tail produced.
单核细胞增生李斯特菌被用作细胞内寄生模型,以研究细菌在巨噬细胞系中的侵入、生长、移动和扩散阶段。感染的第一步是单核细胞增生李斯特菌被吞噬,随后吞噬体周围的膜溶解,推测这是由单核细胞增生李斯特菌分泌的溶血素介导的,因为非溶血突变体仍留在完整的液泡中。感染后2小时内,每个现在位于细胞质中的单核细胞增生李斯特菌被肌动蛋白丝包裹,通过用肌球蛋白亚片段1装饰肌动蛋白丝来识别。这些丝非常短。单核细胞增生李斯特菌生长并分裂,肌动蛋白丝重新排列形成一条长尾巴(通常长5微米),仅从细菌的一端伸出,即“彗尾”,其中肌动蛋白丝呈现随机排列。单核细胞增生李斯特菌“彗星”以其尾巴朝向细胞中心的方向移动到细胞表面,并被纳入细胞突起中,单核细胞增生李斯特菌位于突起的顶端,其尾巴拖入其后面的细胞质中。这个突起与相邻的巨噬细胞接触,该巨噬细胞吞噬第一个巨噬细胞的突起。因此,在第二个巨噬细胞的细胞质中是一个单核细胞增生李斯特菌,其肌动蛋白尾巴被一层膜包围,而这层膜又被新宿主的吞噬体膜包围。然后这两层膜都被单核细胞增生李斯特菌溶解,循环重复。因此,一旦进入宿主细胞,感染的单核细胞增生李斯特菌及其后代可以通过保持在细胞内而在细胞间传播,从而绕过机体的体液免疫系统。为了确定肌动蛋白丝对于单核细胞增生李斯特菌在细胞间传播是否至关重要,我们用细胞松弛素D处理感染的巨噬细胞。单核细胞增生李斯特菌不仅未能传播,而且大多数位于细胞质深处,而不是靠近细胞周边。超薄切片显示没有形成肌动蛋白丝网络,也没有产生“彗尾”。