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首页> 外文期刊>Infection and immunity >Signal Transduction during Legionella pneumophila Entry into Human Monocytes
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Signal Transduction during Legionella pneumophila Entry into Human Monocytes

机译：嗜肺军团菌进入人单核细胞过程中的信号转导

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Legionella pneumophila causes Legionnaires’ disease by replication in alveolar macrophages and monocytes. The bacteria are internalized most efficiently by opsonin-dependent, CR3-mediated phagocytosis. This investigation focused on determining the role of actin polymerization and phosphorylation signals in this uptake mechanism. Uptake inhibition assays and confocal microscopic analysis indicated that entry of L. pneumophila activated tyrosine kinase (TK) and protein kinase C (PKC) and induced actin polymerization at the site of bacterial entry. Upon L. pneumophila entry, six major cellular proteins (75, 71, 59, 56, 53, and 52 kDa) were TK phosphorylated in soluble fractions of monocytes, and three of these proteins (52, 53, and 56 kDa) were consistently found in insoluble (i.e., cytoskeletal) fractions of monocytes as well. Tyrosine phosphorylation was suppressed when cells were pretreated with the kinase inhibitor genistein, tyrphostin, or staurosporine. A similar tyrosine-phosphorylated protein pattern was observed with CR3-mediated entry of avirulent L. pneumophila, Escherichia coli, or zymosan into monocytes. This study has shown that PKC and TK signals which activate actin polymerization during the process of phagocytosis are induced upon L. pneumophila entry. In addition, CR3 receptor-mediated phagocytosis into monocytes may involve tyrosine phosphorylation of similar proteins, regardless of the particle being phagocytosed. Therefore, the tyrosine-induced phosphorylation observed during opsonized L. pneumophilaentry is not a virulence-associated event.
机译：嗜肺军团杆菌通过在肺泡巨噬细胞和单核细胞中复制而导致退伍军人症。细菌通过调理素依赖性CR3介导的吞噬作用最有效地内化。这项研究的重点是确定肌动蛋白聚合和磷酸化信号在这种摄取机制中的作用。摄取抑制测定和共聚焦显微镜分析表明 L的进入。肺炎支气管炎激活酪氨酸激酶（TK）和蛋白激酶C（PKC），并在细菌进入部位诱导肌动蛋白聚合。在 L。肺炎支原体进入时，六种主要细胞蛋白（75、71、59、56、53和52 kDa）在单核细胞的可溶级分中被TK磷酸化，其中三种蛋白（52、53和56 kDa）为在单核细胞的不溶性（即，细胞骨架）部分中也始终存在。当用激酶抑制剂染料木黄酮，酪氨酸蛋白酶抑制剂或星形孢菌素预处理细胞时，酪氨酸磷酸化被抑制。在CR3介导的无毒 L进入中观察到相似的酪氨酸磷酸化蛋白质模式。肺炎，大肠杆菌或酵母聚糖进入单核细胞。该研究表明， L诱导了在吞噬过程中激活肌动蛋白聚合的PKC和TK信号。肺炎条目。此外，CR3受体介导的单核细胞吞噬作用可能涉及相似蛋白质的酪氨酸磷酸化，而不管被吞噬的颗粒如何。因此，在调理的 L期间观察到酪氨酸诱导的磷酸化。肺炎支原体不是毒力相关事件。

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