Inducible nitric oxide synthase protection against coxsackievirus pancreatitis.
Inducible nitric oxide synthase protection against coxsackievirus pancreatitis.
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DOI：
10.4049/jimmunol.163.10.5497
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发表时间：
1999-11
影响因子：
4.4
通讯作者：
C. Zaragoza;C. J. Ocampo;M. Saura;C. Bao;M. Leppo;A. Lafond-Walker;D. Thiemann;R. Hruban;C. Lowenstein
中科院分区：
文献类型：
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作者：
C. Zaragoza;C. J. Ocampo;M. Saura;C. Bao;M. Leppo;A. Lafond-Walker;D. Thiemann;R. Hruban;C. Lowenstein
柯萨奇病毒感染可引起人类心肌炎和胰腺炎。在某些小鼠品系中，柯萨奇病毒引起严重的胰腺炎。我们探讨了NO在宿主对病毒性胰腺炎免疫反应中的作用。柯萨奇病毒在缺乏NO合酶2 （NOS2）的小鼠中复制到比野生型小鼠更高的滴度，在胰腺中具有特别高的病毒滴度和病毒RNA水平。缺乏NOS的小鼠有严重的坏死性胰腺炎，血液中胰腺酶升高，腺泡细胞坏死。缺乏NOS2导致感染小鼠的死亡率迅速增加。因此，NOS2在柯萨奇病毒感染的免疫应答中是一个关键的组成部分。
Coxsackievirus infection causes myocarditis and pancreatitis in humans. In certain strains of mice, Coxsackievirus causes a severe pancreatitis. We explored the role of NO in the host immune response to viral pancreatitis. Coxsackievirus replicates to higher titers in mice lacking NO synthase 2 (NOS2) than in wild-type mice, with particularly high viral titers and viral RNA levels in the pancreas. Mice lacking NOS have a severe, necrotizing pancreatitis, with elevated pancreatic enzymes in the blood and necrotic acinar cells. Lack of NOS2 leads to a rapid increase in the mortality of infected mice. Thus, NOS2 is a critical component in the immune response to Coxsackievirus infection.