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首页> 外文期刊>Infection and immunity >Increases in c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase and p38 Activity in Monocyte-Derived Macrophages following the Uptake of Legionella pneumophila
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Increases in c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase and p38 Activity in Monocyte-Derived Macrophages following the Uptake of Legionella pneumophila

机译：嗜肺军团菌摄取后单核细胞衍生巨噬细胞中c-Jun N末端激酶/应力激活蛋白激酶和p38活性的增加

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Legionella pneumophila, the causative agent of Legionnaires' disease, infects and replicates within a variety of eukaryotic cells. The purpose of the current study was to examine host cell signaling events immediately following uptake and early in the endocytic process (less than 1 h) following the phagocytosis of L. pneumophila. This examination focused on the protein kinase signal pathways to identify any aberrant signal(s) induced by L. pneumophila within its host, as a means to alter the normal endocytic pathway. The mitogen-activated protein kinase cascades are of interest due to their involvement in cellular regulation. The experiments were carried out with monocyte-derived macrophages (MDMs). All three mitogen-activated protein kinase cascades were activated when MDMs were inoculated with either Legionella strain (wild-type strain AA100 or dotA mutant GL10) or an Escherichia coli control. Whereas the avirulent treatments, GL10 and E. coli, exhibited a leveling off or a return to near basal levels of phosphorylation/activity of c-Jun N-terminal kinase by 60 min, the virulent strain AA100 exhibited a significantly increased level of activity through 60 min that was greater than that seen in GL10 (P = 0.025) and E. coli (P = 0.014). A similar trend was seen with p38 phosphorylation. Phosphorylation of mitogen-activated protein/ERK kinase (MEK) was decreased in strain AA100 compared to E. coli. Inhibition of the activity of either the stress-activated protein kinase/c-Jun N-terminal kinase or p38 pathway significantly decreased the ability of legionellae to replicate intracellularly, suggesting the necessity of these two pathways in its intracellular survival and replication.
机译：军团菌病的致病菌 Legionella pneumophila 感染并在多种真核细胞中复制。本研究的目的是检查摄取后立即和吞噬 L后内吞过程的早期（少于1小时）的宿主细胞信号事件。肺炎。这项检查的重点是蛋白激酶信号通路，以鉴定由 L诱导的任何异常信号。宿主内的嗜肺性肺炎，以改变正常的内吞途径。促分裂原活化的蛋白激酶级联反应由于其参与细胞调节而受到关注。用单核细胞衍生的巨噬细胞（MDM）进行实验。当用 Legionella 菌株（野生型AA100或 dotA 突变体GL10）或大肠杆菌接种MDM时，所有三个促分裂原激活的蛋白激酶级联反应均被激活。 控件。而无毒的处理剂GL10和 E。大肠杆菌，到60分钟时，其c-Jun N端激酶的磷酸化/活性水平趋于稳定或恢复到接近基本水平，而强毒株AA100在60分钟内的活性水平却显着提高，比GL10（ P = 0.025）和 E中看到的要好。大肠杆菌（ P = 0.014）。 p38磷酸化也观察到类似的趋势。与 E相比，AA100菌株中丝裂原活化蛋白/ ERK激酶（MEK）的磷酸化降低。大肠杆菌。抑制压力激活的蛋白激酶/ c-Jun N-末端激酶或p38途径的活性会显着降低军团菌在细胞内复制的能力，表明这两种途径在其细胞内存活和复制中是必要的。

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