一氧化氮抑制小鼠心肌炎中的病毒复制。
Nitric oxide inhibits viral replication in murine myocarditis.
作者信息
Lowenstein C J, Hill S L, Lafond-Walker A, Wu J, Allen G, Landavere M, Rose N R, Herskowitz A
机构信息
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
出版信息
J Clin Invest. 1996 Apr 15;97(8):1837-43. doi: 10.1172/JCI118613.
Abstract
Nitric oxide (NO) is a radical molecule that not only serves as a vasodilator and neurotransmitter but also acts as a cytotoxic effector molecule of the immune system. The inducible enzyme making NO, inducible NO synthase (iNOS), is transcriptionally activated by IFN-gamma and TNF-alpha, cytokines which are produced during viral infection. We show that iNOS is induced in mice infected with the Coxsackie B3 virus. Macrophages expressing iNOS are identified in the hearts and spleens of infected animals with an antibody raised against iNOS. Infected mice have increased titers of virus and a higher mortality when fed NOS inhibitors. Thus, viral infection induces iNOS in vivo, and NO inhibits viral replication. NO is a novel, nonspecific immune defense against viruses in vivo.
摘要
一氧化氮（NO）是一种自由基分子，它不仅作为血管舒张剂和神经递质发挥作用，还作为免疫系统的细胞毒性效应分子。产生NO的诱导型酶，即诱导型一氧化氮合酶（iNOS），受到γ干扰素和肿瘤坏死因子-α的转录激活，这两种细胞因子是在病毒感染期间产生的。我们发现，感染柯萨奇B3病毒的小鼠体内会诱导iNOS。用针对iNOS产生的抗体在受感染动物的心脏和脾脏中鉴定出表达iNOS的巨噬细胞。当给感染的小鼠喂食一氧化氮合酶抑制剂时，病毒滴度会升高，死亡率也会更高。因此，病毒感染在体内诱导iNOS，而NO抑制病毒复制。NO是体内一种新型的、非特异性的抗病毒免疫防御物质。
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