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首页> 外文期刊>Infection and immunity >Activation and Mitogen-Activated Protein Kinase Regulation of Transcription Factors Ets and NF-κB in Mycobacterium-Infected Macrophages and Role of These Factors in Tumor Necrosis Factor Alpha and Nitric Oxide Synthase 2 Promoter Function
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Activation and Mitogen-Activated Protein Kinase Regulation of Transcription Factors Ets and NF-κB in Mycobacterium-Infected Macrophages and Role of These Factors in Tumor Necrosis Factor Alpha and Nitric Oxide Synthase 2 Promoter Function

机译：转录因子ETS和NF-κB在分枝杆菌感染巨噬细胞中的激活和丝裂原激活蛋白激酶调节及其在肿瘤坏死因子α和一氧化氮合酶2启动子功能中的作用

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Previous studies have shown that primary murine macrophages infected with Mycobacterium avium produced lower levels of tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase 2 (NOS2) compared to cells infected with nonpathogenic Mycobacterium smegmatis. TNF-α and NOS2 levels correlated with and were dependent on the activation of mitogen-activated protein kinases (MAPKs) p38 and extracellular signal-regulated kinase 1/2 (ERK1/2). To define the macrophage transcriptional responses dependent on ERK1/2 activation following a mycobacterial infection, we used RAW 264.7 cells transfected with a TNF-α or NOS2 promoter vector. We determined that macrophages infected with M. avium compared to M. smegmatis showed diminished TNF-α and NOS2 promoter activity. A more pronounced difference in promoter activity was observed when only the consensus ETS and NF-κB binding sites were used as promoters. Mutational analysis of the ETS and NF-κB binding sites present on the TNF-α and NOS2 promoters, respectively, showed that these sites were essential for a functional promoter. Moreover, the Ets/Elk but not the NF-κB transcriptional response was dependent on ERK1/2. This correlated with the requirement for ERK1/2 in TNF-α but not NOS2 promoter activity. Our data indicate that the increased Ets/Elk and NF-κB promoter activities associated with M. smegmatis-infected macrophages are responsible, at least in part, for the increased TNF-α and NOS2 production observed in these infected cells and that ERK1/2 is required for Ets/Elk activity and full TNF-α production.
机译：以前的研究表明，与感染非对比感染的细胞相比，用Hycocobacterium Avium 产生较低水平的肿瘤坏死因子α（TNF-α）和诱导型一氧化氮合酶2（NOS2）的初级鼠巨噬细胞分枝杆菌smogmatis 。 TNF-α和NOS2水平与并依赖于丝裂原激活蛋白激酶（MAPK）P38和细胞外信号调节激酶1/2（ERK1 / 2）的活化。为了定义依赖于分枝杆菌感染后依赖于ERK1 / 2活化的巨噬细胞转录反应，我们使用用TNF-α或NOS2启动子载体转染的原料264.7细胞。我们确定巨噬细胞感染 m。 Avium 与 M相比。 Smogmatis 显示TNF-α和NOS2启动子活性减少。观察到在仅使用共有ETS和NF-κB结合位点作为启动子时观察到启动子活性的更明显的差异。分别在TNF-α和NOS2启动子上的ETS和NF-κB结合位点的突变分析表明这些位点对于官能启动子是必不可少的。此外，ETS / ELK但不是NF-κB转录响应依赖于ERK1 / 2。这与TNF-α中ERK1 / 2的要求相关，但不是NOS2启动子活性。我们的数据表明，与 M相关的ETS / ELK和NF-κB启动子活动增加。 Smogmatis -Infected巨噬细胞至少部分地负责，对于在这些感染的细胞中观察到的增加的TNF-α和NOS2产生，并且ETK1 / 2需要ETS / ELK活性和全TNF-α产生。

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