Khaiboullina S F, Netski D M, Krumpe P, St Jeor S C
Department of Microbiology and Cell and Molecular Biology Program, School of Medicine, University of Nevada-Reno, Reno, Nevada 89557, USA.
J Virol. 2000 Dec;74(24):11966-71. doi: 10.1128/jvi.74.24.11966-11971.2000.
Previous data indicate that immune mechanisms may be involved in developing capillary leakage during Sin Nombre virus (SNV) infection. Therefore, we investigated production of tumor necrosis factor alpha (TNF-alpha) by human alveolar macrophages and human umbilical vein endothelial cells (HUVEC) after infection with SNV. In addition, we examined the effect of TNF-alpha on HUVEC monolayer leakage. Our results reveal that although TNF-alpha decreases accumulation of viral nucleoproteins, TNF-alpha levels do not change in SNV-infected cells. In addition, supernatants from SNV-infected human alveolar macrophages did not cause a significant increase in endothelial monolayer permeability.
先前的数据表明，免疫机制可能参与了汉坦病毒（SNV）感染期间毛细血管渗漏的发生。因此，我们研究了人肺泡巨噬细胞和人脐静脉内皮细胞（HUVEC）在感染SNV后肿瘤坏死因子α（TNF-α）的产生情况。此外，我们还检测了TNF-α对HUVEC单层渗漏的影响。我们的结果显示，虽然TNF-α可减少病毒核蛋白的积累，但在感染SNV的细胞中TNF-α水平并未改变。此外，感染SNV的人肺泡巨噬细胞的上清液并未导致内皮单层通透性显著增加。
