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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Protein kinase C δ is essential for optimal macrophage-mediated phagosomal containment of Listeria monocytogenes
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Protein kinase C δ is essential for optimal macrophage-mediated phagosomal containment of Listeria monocytogenes

机译：蛋白激酶Cδ对于巨噬细胞介导的单核细胞增生李斯特菌吞噬体的最佳遏制至关重要

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Activation of macrophages and subsequent "killing" effector functions against infectious pathogens are essential for the establishment of protective immunity. NF-IL6 is a transcription factor downstream of IFN-γ and TNF in the macrophage activation pathway required for bacterial killing. Comparison of microarray expression profiles of Listeria monocytogenes (LM)-infected macrophages from WT and NF-IL6-deficient mice enabled us to identify candidate genes downstream of NF-IL6 involved in the unknown pathways of LM killing independent of reactive oxygen intermediates and reactive nitrogen intermediates. One differentially expressed gene, PKCδ, had higher mRNA levels in the LM-infected NF-IL6-deficient macrophages as compared with WT. To define the role of PKCδ during listeriosis, we infected PKCδ-deficient mice with LM. PKCδ-deficient mice were highly susceptible to LM infection with increased bacterial burden and enhanced histopathology despite enhanced NF-IL6 mRNA expression. Subsequent studies in PKCδ-deficient macrophages demonstrated that, despite elevated levels of proinflammatory cytokines and NO production, increased escape of LM from the phagosome into the cytoplasm and uncontrolled bacterial growth occurred. Taken together these data identified PKCδ as a critical factor for confinement of LM within macrophage phagosomes.
机译：巨噬细胞的激活以及随后针对感染性病原体的“杀死”效应子功能对于建立保护性免疫至关重要。 NF-IL6是细菌杀死所需的巨噬细胞激活途径中IFN-γ和TNF下游的转录因子。 WT和NF-IL6缺陷小鼠感染单核细胞增生性李斯特菌（LM）的巨噬细胞微阵列表达谱的比较使我们能够鉴定NF-IL6下游的候选基因，这些基因参与了LM杀死未知途径，而与活性氧中间体和活性氮无关中间体。与野生型相比，在LM感染的NF-IL6缺陷型巨噬细胞中，一个差异表达的基因PKCδ具有更高的mRNA水平。为了确定李斯特菌病中PKCδ的作用，我们用LM感染了PKCδ缺陷的小鼠。尽管NF-IL6 mRNA表达增强，但PKCδ缺陷型小鼠高度易受LM感染，增加细菌负担并增强组织病理学。随后对PKCδ缺陷型巨噬细胞的研究表明，尽管促炎性细胞因子水平升高和NO产生，LM从吞噬体进入细胞质的逸出增加，并且细菌生长不受控制。这些数据加在一起确定PKCδ是限制巨噬细胞吞噬体内的LM的关键因素。

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