Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Minas Gerais, CEP 31270-901, Brazil.
Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Minas Gerais, CEP 31270-901, Brazil.
J Cell Sci. 2019 Mar 25;132(6):jcs226183. doi: 10.1242/jcs.226183.
Intracellular parasites of the genus are the causative agents of leishmaniasis. The disease is transmitted by the bite of a sand fly vector, which inoculates the parasite into the skin of mammalian hosts, including humans. During chronic infection the parasite lives and replicates inside phagocytic cells, notably the macrophages. An interesting, but overlooked finding, is that other cell types and even non-phagocytic cells have been found to be infected by spp. Nevertheless, the mechanisms by which invades such cells had not been previously studied. Here, we show that can induce their own entry into fibroblasts independently of actin cytoskeleton activity, and, thus, through a mechanism that is distinct from phagocytosis. Invasion involves subversion of host cell functions, such as Ca signaling and recruitment and exocytosis of host cell lysosomes involved in plasma membrane repair.This article has an associated First Person interview with the first author of the paper.
属于 的细胞内寄生虫是利什曼病的病原体。这种疾病通过沙蝇媒介的叮咬传播，沙蝇将寄生虫接种到包括人类在内的哺乳动物宿主的皮肤中。在慢性感染期间，寄生虫在吞噬细胞内生存和复制，特别是巨噬细胞。一个有趣但被忽视的发现是，其他细胞类型甚至非吞噬细胞也被发现被 spp 感染。然而，以前尚未研究过 进入此类细胞的机制。在这里，我们表明 可以在不依赖肌动蛋白细胞骨架活性的情况下独立诱导自身进入成纤维细胞，因此，它通过一种与吞噬作用不同的机制。入侵涉及宿主细胞功能的颠覆，例如 Ca 信号转导以及参与质膜修复的宿主细胞溶酶体的募集和胞吐作用。本文有与本文第一作者的相关第一人称采访。
