Effects of tumor necrosis factor alpha on Sin Nombre virus infection in vitro
Effects of tumor necrosis factor alpha on Sin Nombre virus infection in vitro
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DOI：
10.1128/jvi.74.24.11966-11971.2000
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发表时间：
2000-12-01
影响因子：
5.4
通讯作者：
St Jeor, SC
中科院分区：
文献类型：
--
作者：
Khaiboullina, SF;Netski, DM;St Jeor, SC
以往的数据表明，免疫机制可能参与了新诺布雷病毒(SNV)感染过程中毛细血管渗漏的发生。因此，我们研究了SNV感染后人肺泡巨噬细胞和人脐静脉内皮细胞产生肿瘤坏死因子-α(TNF-α)的情况。此外，我们还检测了肿瘤坏死因子-α对血管内皮细胞单层渗漏的影响。我们的结果表明，尽管肿瘤坏死因子-α减少了病毒核蛋白的积累，但在SNV感染的细胞中，肿瘤坏死因子-α的水平没有变化。此外，SNV感染的人肺泡巨噬细胞的上清液不会引起内皮细胞单层通透性的显著增加。
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.