Tardieux I, Webster P, Ravesloot J, Boron W, Lunn J A, Heuser J E, Andrews N W
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
Cell. 1992 Dec 24;71(7):1117-30. doi: 10.1016/s0092-8674(05)80061-3.
Trypanosoma cruzi invades most nucleated cells by a mechanism distinct from classical phagocytosis. Although parasites enter at the lysosome-poor peripheral cell margins, lysosomal markers are immediately incorporated into the parasitophorous vacuole. No accumulation of polymerized actin was detected around recently internalized parasites, and disruption of microfilaments significantly facilitated invasion. Lysosomes were observed to aggregate at the sites of trypanosome attachment and to fuse with the vacuole at early stages of its formation. Experimentally induced, microtubule-dependent movement of lysosomes from the perinuclear area to the cell periphery enhanced entry. Conditions that deplete cells of peripheral lysosomes or interfere with lysosomal fusion capacity inhibited invasion. These observations reveal a novel mechanism for cell invasion:recruitment of lysosomes for fusion at the site of parasite internalization.
克氏锥虫通过一种不同于经典吞噬作用的机制侵入大多数有核细胞。尽管寄生虫在溶酶体较少的细胞周边边缘进入，但溶酶体标记物会立即被纳入寄生泡。在最近内化的寄生虫周围未检测到聚合肌动蛋白的积累，微丝的破坏显著促进了入侵。观察到溶酶体在锥虫附着部位聚集，并在其形成的早期阶段与液泡融合。实验诱导的溶酶体从核周区域向细胞周边的微管依赖性运动增强了进入。耗尽细胞周边溶酶体或干扰溶酶体融合能力的条件会抑制入侵。这些观察结果揭示了一种新的细胞入侵机制：在寄生虫内化部位募集溶酶体进行融合。
