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诱导型一氧化氮合酶对柯萨奇病毒胰腺炎的保护作用。

Inducible nitric oxide synthase protection against coxsackievirus pancreatitis.

作者信息

Zaragoza C, Ocampo C J, Saura M, Bao C, Leppo M, Lafond-Walker A, Thiemann D R, Hruban R, Lowenstein C J

机构信息

Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

J Immunol. 1999 Nov 15;163(10):5497-504.

PMID:10553076
Abstract

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.

摘要

柯萨奇病毒感染可导致人类患心肌炎和胰腺炎。在某些品系的小鼠中,柯萨奇病毒会引发严重的胰腺炎。我们探究了一氧化氮(NO)在宿主对病毒性胰腺炎免疫反应中的作用。与野生型小鼠相比,缺乏一氧化氮合酶2(NOS2)的小鼠体内柯萨奇病毒的复制滴度更高,胰腺中的病毒滴度和病毒RNA水平尤其高。缺乏NOS的小鼠会患严重的坏死性胰腺炎,血液中胰腺酶水平升高,腺泡细胞坏死。缺乏NOS2会导致感染小鼠的死亡率迅速上升。因此,NOS2是宿主对柯萨奇病毒感染免疫反应的关键组成部分。

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