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首页> 外文期刊>Infection and immunity >Interaction of Listeria monocytogenes with mouse dendritic cells.
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Interaction of Listeria monocytogenes with mouse dendritic cells.

机译：李斯特菌与小鼠树突状细胞的相互作用。

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In this study, the interaction of murine dendritic cells with Listeria monocytogenes was investigated. Dendritic cells are efficient antigen-presenting cells, play a key role in the immune response, and are capable of migrating over substantial distances between sites of infection and lymphoid tissues. L. monocytogenes EGD invaded dendritic cells, escaped from phagosomes into the cytoplasm, and there directed actin nucleation, polymerization, and polarization in a typical fashion, thereby achieving intracellular movement and cell-to-cell spread. The internalization process appears to be independent of the inl locus. Interestingly, an intact microtubular function was essential for efficient uptake, whereas in a previous report, microtubule disruption did not affect bacterial spread in Caco-2 cells. The results obtained also suggest that L. monocytogenes binds to glycosylated receptors of dendritic cells. Uptake of Listeria cells was mediated by a protein kinase-dependent transducing phosphorylation signal that induces the actin polymerization-dependent phagocytic process. To achieve efficient uptake, de novo protein synthesis of eukaryotic and prokaryotic cells is also required. Despite the killing of dendritic cells, wild-type bacteria were found to persist in small numbers in some cells for at least 24 h. When different isogenic mutants of the EGD strain were analyzed for their capability to interact with dendritic cells, it was observed that some virulence-attenuated mutants (i.e., prfA and delta hly) persisted in large numbers for even longer times. Invasion of dendritic cells by L. monocytogenes, which in turn could result in either cell death or persistent infection, might have an important role in the pathogenesis of listeriosis, leading to impaired immune responses with inefficient bacterial clearance and/or promoting bacterial spread.
机译：在这项研究中，研究了鼠树突状细胞与单核细胞增生性李斯特菌的相互作用。树突状细胞是有效的抗原呈递细胞，在免疫反应中起关键作用，并且能够在感染部位和淋巴组织之间的相当长的距离上迁移。单核细胞增生李斯特氏菌EGD侵入树突状细胞，从吞噬体逃逸到细胞质中，并以典型方式指导肌动蛋白成核，聚合和极化，从而实现细胞内移动和细胞间扩散。内部化过程似乎与inl基因座无关。有趣的是，完整的微管功能对于有效摄取至关重要，而在以前的报告中，微管破坏并不影响细菌在Caco-2细胞中的扩散。获得的结果还表明，单核细胞增生李斯特菌与树突状细胞的糖基化受体结合。李斯特菌细胞的摄取是由蛋白激酶依赖性转导的磷酸化信号介导的，该信号诱导肌动蛋白聚合依赖性吞噬过程。为了实现有效摄取，还需要真核和原核细胞的从头蛋白质合成。尽管杀死了树突状细胞，但发现野生型细菌在一些细胞中仍会持续至少24小时。当分析EGD菌株的不同等基因突变体与树突状细胞相互作用的能力时，观察到一些毒力减弱的突变体（即，prfA和Δhly）大量持续甚至更长的时间。单核细胞增生李斯特氏菌入侵树突状细胞反过来可能导致细胞死亡或持续感染，这可能在李斯特菌病的发病机理中起重要作用，导致免疫应答受损，细菌清除效率低下和/或促进细菌扩散。

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