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首页> 外文期刊>Microbiology and Immunology >Autocrine interferon-beta stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected with herpes simplex virus type 1.
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Autocrine interferon-beta stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected with herpes simplex virus type 1.

机译:自分泌干扰素-β刺激增加了感染1型单纯疱疹病毒的小鼠巨噬细胞J774A.1细胞产生的一氧化氮。

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The pathogenic roles of nitric oxide (NO) in mouse models have been reported for herpes simplex virus type 1 (HSV-1)-induced pneumonia as well as endotoxin shock. We compared the mechanism of NO production induced by HSV-1 with that induced by lipopolysaccharide (LPS) using a mouse macrophage cell line, J774A.1. Both HSV-1 and LPS induced NO production as well as antiviral activity, which were attenuated by anti-interferon (IFN)-beta treatment. These results suggest that autocrine IFN-beta plays a role in NO release by J774A.1 cells stimulated with HSV-1 or LPS.
机译:一氧化氮(NO)在小鼠模型中的致病作用据报道对于1型单纯疱疹病毒(HSV-1)诱发的肺炎以及内毒素休克。我们使用小鼠巨噬细胞系J774A.1比较了HSV-1诱导的NO产生与脂多糖(LPS)诱导的NO产生的机制。 HSV-1和LPS均可诱导NO产生以及抗病毒活性,这些活性被抗干扰素(IFN)-β处理减弱。这些结果表明,自分泌IFN-β在被HSV-1或LPS刺激的J774A.1细胞释放NO方面发挥了作用。

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