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Toxoplasma gondii Mechanisms of Entry Into Host Cells.
Frontiers in Cellular and Infection Microbiology ( IF 5.7 ) Pub Date : 2020-05-19 , DOI: 10.3389/fcimb.2020.00294
Juliana Portes 1, 2 , Emile Barrias 3 , Renata Travassos 1, 2 , Márcia Attias 1, 2 , Wanderley de Souza 1, 2
Affiliation  

Toxoplasma gondii, the causative agent of toxoplasmosis, is an obligate intracellular protozoan parasite. Toxoplasma can invade and multiply inside any nucleated cell of a wide range of homeothermic hosts. The canonical process of internalization involves several steps: an initial recognition of the host cell surface and a sequential secretion of proteins from micronemes followed by rhoptries that assemble a macromolecular complex constituting a specialized and transient moving junction. The parasite is then internalized via an endocytic process with the establishment of a parasitophorous vacuole (PV), that does not fuse with lysosomes, where the parasites survive and multiply. This process of host cell invasion is usually referred to active penetration. Using different cell types and inhibitors of distinct endocytic pathways, we show that treatment of host cells with compounds that interfere with clathrin-mediated endocytosis (hypertonic sucrose medium, chlorpromazine hydrochloride, and pitstop 2 inhibited the internalization of tachyzoites). In addition, treatments that interfere with macropinocytosis, such as incubation with amiloride or IPA-3, increased parasite attachment to the host cell surface but significantly blocked parasite internalization. Immunofluorescence microscopy showed that markers of macropinocytosis, such as the Rab5 effector rabankyrin 5 and Pak1, are associated with parasite-containing cytoplasmic vacuoles. These results indicate that entrance of T. gondii into mammalian cells can take place both by the well-characterized interaction of parasite and host cell endocytic machinery and other processes, such as the clathrin-mediated endocytosis, and macropinocytosis.



中文翻译:

弓形虫进入宿主细胞的机制。

弓形虫弓形虫病的病原体是专性的细胞内原生动物寄生虫。 弓形虫可以侵袭各种各样的等温宿主的任何有核细胞。内在化的规范化过程涉及几个步骤:宿主细胞表面的初步识别和从微neme的蛋白质的顺序分泌,然后是组装构成大分子复合物的rhoptry,构成一个专门的和短暂的运动连接。然后,通过内吞过程将寄生虫内化,建立了一个不与溶酶体融合的寄生虫液泡(PV),寄生虫在那里存活并繁殖。宿主细胞入侵的过程通常称为主动渗透。使用不同的细胞类型和不同的内吞途径抑制剂,我们证明了用干扰网格蛋白介导的内吞作用的化合物(高渗蔗糖培养基,盐酸氯丙嗪和pitstop 2抑制了速殖子的内在化。此外,干扰巨胞饮作用的处理(例如与阿米洛利或IPA-3孵育)会增加寄生虫与宿主细胞表面的附着,但会显着阻止寄生虫的内在化。免疫荧光显微镜检查显示,巨细胞增多症的标志物,如Rab5效应分子rabankyrin 5和Pak1,与含有寄生虫的细胞质液泡有关。这些结果表明 免疫荧光显微镜检查显示,巨细胞增多症的标志物,如Rab5效应分子rabankyrin 5和Pak1,与含有寄生虫的细胞质液泡有关。这些结果表明 免疫荧光显微镜检查显示,巨细胞增多症的标志物,如Rab5效应分子rabankyrin 5和Pak1,与含有寄生虫的细胞质液泡有关。这些结果表明弓形虫 进入哺乳动物细胞既可以通过寄生虫与宿主细胞内吞机制的充分表征的相互作用,也可以通过其他过程(例如网格蛋白介导的内吞作用和巨胞饮作用)发生。

更新日期:2020-06-30
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