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首页> 外文期刊>Infection and immunity >Lamellipodin Is Important for Cell-to-Cell Spread and Actin-Based Motility in Listeria monocytogenes
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Lamellipodin Is Important for Cell-to-Cell Spread and Actin-Based Motility in Listeria monocytogenes

机译：Lamellipodin对于单核细胞增生李斯特菌中的细胞间传播和基于肌动蛋白的运动很重要

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Listeria monocytogenes is a foodborne pathogen capable of invading a broad range of cell types and replicating within the host cell cytoplasm. This paper describes the colocalization of host cell lamellipodin (Lpd) with intracellular L. monocytogenes detectable 6 h postinfection of epithelial cells. The association was mediated via interactions between both the peckstrin homology (PH) domain in Lpd and phosphatidylinositol (3,4)-bisphosphate [PI(3,4)P2] on the bacterial surface and by interactions between the C-terminal EVH1 (Ena/VASP [vasodilator-stimulated phosphoprotein] homology domain 1) binding domains of Lpd and the host VASP (vasodilator-stimulated phosphoprotein) recruited to the bacterial cell surface by the listerial ActA protein. Depletion of Lpd by short interfering RNA (siRNA) resulted in reduced plaque size and number, indicating a role for Lpd in cell-to-cell spread. In contrast, overexpression of Lpd resulted in an increase in the number of L. monocytogenes-containing protrusions (listeriopods). Manipulation of the levels of Lpd within the cell also affected the intracellular velocity of L. monocytogenes, with a reduction in Lpd corresponding to an increase in intracellular velocity. These data, together with the observation that Lpd accumulated at the interface between the bacteria and the developing actin tail at the initiation of actin-based movement, indicate a possible role for Lpd in the actin-based movement and the cell-to-cell spread of L. monocytogenes.
机译：单核细胞增生性李斯特菌是一种食源性病原体，能够侵袭多种细胞类型并在宿主细胞质内复制。本文描述了宿主细胞lamellipodin（Lpd）与细胞内单核细胞增生李斯特氏菌在感染上皮细胞后6小时可共定位。这种联系是通过Lpd中的peckstrin同源（PH）域与磷脂酰肌醇（3,4）-双磷酸[PI（3,4）P 2 ]之间的相互作用和相互作用介导的。 Lpd的C端EVH1（Ena / VASP [血管扩张剂刺激的磷蛋白]同源结构域1）结合结构域与由李斯特菌ActA蛋白募集到细菌细胞表面的宿主VASP（血管扩张剂刺激的磷蛋白）之间。短干扰RNA（siRNA）消耗Lpd导致噬菌斑大小和数量减少，表明Lpd在细胞间扩散中发挥了作用。相反，Lpd的过表达导致含有单核细胞增生李斯特氏菌的突起（李斯特类）的数量增加。对细胞内Lpd水平的操纵也影响了单核细胞增生李斯特菌的细胞内速度，Lpd的减少与细胞内速度的增加相对应。这些数据，以及在基于肌动蛋白的运动开始时Lpd累积在细菌和发育中的肌动蛋白尾巴之间的界面上的观察结果，表明Lpd在基于肌动蛋白的运动和细胞间扩散中可能发挥作用单核细胞增生李斯特菌。

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