Benencia F, Courreges M C
Department of Biological Chemistry, Faculty of Sciences, University of Buenos Aires, Ciudad Universitaria, Argentina.
Immunology. 1999 Nov;98(3):363-70. doi: 10.1046/j.1365-2567.1999.00864.x.
In this study we evaluated the relationship between nitric oxide (NO) and macrophage antiviral extrinsic activity. Macrophages activated by intraperitoneal injection of herpes simplex virus-2 (HSV-2), showed both extrinsic antiviral activity and high nitrite production in contrast to non-activated, resident macrophages. The extrinsic antiviral activity was observed in cultures of Vero cells infected with HSV-1 and HSV-2. The NO inhibitor N-monomethyl-l-arginine acetate (l-NMA) impaired the antiviral activity of HSV-elicited macrophages. The effect was dose dependent and correlated with a reduction of nitrite in the culture media. The effect of l-NMA was reversed by the addition of l-arginine. These data indicate that NO could be responsible for the described activity. Furthermore, l-NMA treatment resulted in the aggravation of HSV-1-induced keratitis in the mouse model, supporting a defensive role of NO in the pathogenesis of HSV-1 corneal infection.
在本研究中，我们评估了一氧化氮（NO）与巨噬细胞抗病毒外在活性之间的关系。与未激活的驻留巨噬细胞相比，通过腹腔注射单纯疱疹病毒2型（HSV-2）激活的巨噬细胞既表现出外在抗病毒活性，又有高亚硝酸盐生成。在用HSV-1和HSV-2感染的Vero细胞培养物中观察到了外在抗病毒活性。NO抑制剂N-单甲基-L-精氨酸乙酸盐（L-NMA）损害了HSV诱导的巨噬细胞的抗病毒活性。该效应呈剂量依赖性，且与培养基中亚硝酸盐的减少相关。添加L-精氨酸可逆转L-NMA的作用。这些数据表明NO可能是所述活性的原因。此外，L-NMA处理导致小鼠模型中HSV-1诱导的角膜炎加重，支持了NO在HSV-1角膜感染发病机制中的防御作用。
