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首页> 外文期刊>Infection and immunity >Intracellular and cell-to-cell spread of Listeria monocytogenes involves interaction with F-actin in the enterocytelike cell line Caco-2.
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Intracellular and cell-to-cell spread of Listeria monocytogenes involves interaction with F-actin in the enterocytelike cell line Caco-2.

机译：单核细胞增生李斯特菌的细胞内和细胞间传播涉及在肠细胞样细胞系Caco-2中与F-肌动蛋白的相互作用。

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Listeria monocytogenes penetrates and multiplies within professional phagocytes and other cells such as the Caco-2 human enterocytelike cell line. Listeriolysin O, a membrane-damaging cytotoxin accounts for intracellular multiplication through lysis of the membrane-bound phagocytic vacuole. This work demonstrates that once released within the cytosol, L. monocytogenes acquires the capacity to spread intracellularly and infect adjacent cells by interacting with host cell microfilaments. Such evidence was obtained by using drugs which disrupt the cell cytoskeleton. Nocodazole, which blocks polymerization of microtubules, did not affect intracellular spread, whereas cytochalasin D, which blocks polymerization of G-actin, inhibited the intracellular motility of the bacteria. By using fluorescence staining with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin (NBD-phallacidin), transmission electron microscopy, and immunogold labeling, direct evidence was obtained that intracellular bacteria were enveloped with a thick layer of F-actin. Within 2 h after entry, it was demonstrated by confocal microscopy that bacteria were following highly organized routes corresponding to stress fibers. Four hours after entry, some bacteria presented random movements which could be seen by the presence of a large trail of F-actin. Such movements also caused protrusions which deeply penetrated adjacent cells and resulted in the formation of vacuoles limited by a double membrane. After subsequent lysis of these membranes, bacteria released within the cytoplasm were able to multiply and invade new cells. In contrast, an hly::Tn1545 mutant of the wild-type microorganism demonstrated almost no intracellular spread. Only a few bacteria displaying delayed lysis of the phagocytic vacuole behaved like the wild-type strain. Hemolysin-mediated lysis of the phagocytic vacuole and subsequent interaction with host cell microfilaments may represent a major virulence factor allowing tissue colonization during listeriosis.
机译：单核细胞增生性李斯特菌在专业吞噬细胞和其他细胞（例如Caco-2人肠上皮样细胞系）中穿透并繁殖。李斯特菌溶血素O，一种破坏膜的细胞毒素，通过溶解结合在膜上的吞噬液泡来解释细胞内增殖。这项工作表明，单核细胞增生李斯特氏菌一旦在胞质溶胶中释放，便具有与宿主细胞微丝相互作用的能力，使其在细胞内扩散并感染相邻细胞。这些证据是通过使用破坏细胞骨架的药物获得的。阻止微管聚合的诺考达唑不影响细胞内扩散，而阻止G-肌动蛋白聚合的细胞松弛素D抑制细菌的细胞内运动。通过使用7-硝基苯-2-氧杂-1,3-二唑-Phallacidin（NBD-phallacidin）进行荧光染色，透射电镜和免疫金标记，获得了直接的证据，表明细胞内细菌被F-的厚层包裹肌动蛋白。进入后2小时内，通过共聚焦显微镜证明，细菌遵循与应激纤维相对应的高度组织的路径。进入后四个小时，一些细菌呈现出随机运动，这可以通过大量F-肌动蛋白的存在来观察到。这种运动还引起突起，该突起深深地渗透到相邻的细胞中，并形成由双膜限制的液泡。在随后裂解这些膜之后，释放到细胞质内的细菌能够繁殖并侵入新细胞。相反，野生型微生物的hly :: Tn1545突变体几乎没有细胞内扩散。仅少数表现出吞噬液泡裂解延迟的细菌表现得像野生型菌株。溶血素介导的吞噬液泡的裂解以及随后与宿主细胞微丝的相互作用可能代表了主要的毒力因子，允许组织在李斯特菌病期间定植。

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