诱导型一氧化氮合酶在宿主对柯萨奇病毒心肌炎反应中的作用。
The role of inducible nitric oxide synthase in the host response to Coxsackievirus myocarditis.
作者信息
Zaragoza C, Ocampo C, Saura M, Leppo M, Wei X Q, Quick R, Moncada S, Liew F Y, Lowenstein C J
机构信息
Division of Cardiology, Department of Medicine, School of Medicine, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2469-74. doi: 10.1073/pnas.95.5.2469.
Abstract
The host response to Coxsackievirus infection is complex, including T lymphocytes, B lymphocytes, natural killer cells, and macrophages. Although Coxsackievirus infection induces expression of inducible nitric oxide synthase (NOS2; EC 1.14.13.39) in macrophages, the precise role of NOS2 in the host response to Coxsackievirus myocarditis has been unclear. We show, by using mice homozygous for a disrupted NOS2 allele, that Coxsackievirus replicates to higher titers in NOS2(-/-) mice, that the host lacking NOS2 clears virus more slowly than the wild-type host, and that myocarditis is much more severe in infected NOS2(-/-) mice. These data show that NOS2 is crucial for the host response to Coxsackievirus in the mouse.
摘要
机体对柯萨奇病毒感染的反应很复杂，涉及T淋巴细胞、B淋巴细胞、自然杀伤细胞和巨噬细胞。虽然柯萨奇病毒感染可诱导巨噬细胞中诱导型一氧化氮合酶（NOS2；EC 1.14.13.39）的表达，但NOS2在机体对柯萨奇病毒性心肌炎反应中的具体作用尚不清楚。我们通过使用NOS2等位基因缺失的纯合小鼠发现，柯萨奇病毒在NOS2（-/-）小鼠中的复制滴度更高，缺乏NOS2的机体清除病毒的速度比野生型机体更慢，并且感染的NOS2（-/-）小鼠的心肌炎更为严重。这些数据表明，NOS2对小鼠机体对柯萨奇病毒的反应至关重要。
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