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本文引用的文献

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Inhibition of tumor necrosis factor reduces the severity of virus-specific lung immunopathology.肿瘤坏死因子的抑制可降低病毒特异性肺部免疫病理学的严重程度。
Eur J Immunol. 2001 Sep;31(9):2566-73. doi: 10.1002/1521-4141(200109)31:9<2566::aid-immu2566>3.0.co;2-l.
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Characterization of a porcine lung epithelial cell line suitable for influenza virus studies.一种适用于流感病毒研究的猪肺上皮细胞系的特性分析。
J Virol. 2001 Oct;75(19):9517-25. doi: 10.1128/JVI.75.19.9517-9525.2001.
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Bacterial DNA and lipopolysaccharide induce synergistic production of TNF-alpha through a post-transcriptional mechanism.细菌DNA和脂多糖通过转录后机制诱导肿瘤坏死因子-α的协同产生。
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Human peripheral blood T cells, monocytes, and macrophages secrete macrophage inflammatory proteins 1alpha and 1beta following stimulation with heat-inactivated Brucella abortus.人外周血T细胞、单核细胞和巨噬细胞在受到热灭活布鲁氏菌刺激后会分泌巨噬细胞炎性蛋白1α和1β。
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Requirement for STAT1 in LPS-induced gene expression in macrophages.巨噬细胞中LPS诱导基因表达对STAT1的需求。
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Effects of tumor necrosis factor alpha on sin nombre virus infection in vitro.肿瘤坏死因子α对体外汉坦病毒感染的影响。
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The role of alpha/beta and gamma interferons in development of immunity to influenza A virus in mice.α/β干扰素和γ干扰素在小鼠对甲型流感病毒免疫发育中的作用。
J Virol. 2000 May;74(9):3996-4003. doi: 10.1128/jvi.74.9.3996-4003.2000.
8
TNF-alpha inhibits HIV-1 replication in peripheral blood monocytes and alveolar macrophages by inducing the production of RANTES and decreasing C-C chemokine receptor 5 (CCR5) expression.肿瘤坏死因子-α通过诱导调节激活正常T细胞表达和分泌的趋化因子(RANTES)的产生并降低C-C趋化因子受体5(CCR5)的表达,从而抑制外周血单核细胞和肺泡巨噬细胞中的HIV-1复制。
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Production of influenza-stimulated tumor necrosis factor-alpha by monocytes following acute influenza infection in humans.人类急性流感感染后单核细胞产生流感刺激的肿瘤坏死因子-α
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Nasal cytokine and chemokine responses in experimental influenza A virus infection: results of a placebo-controlled trial of intravenous zanamivir treatment.甲型流感病毒实验性感染中的鼻腔细胞因子和趋化因子反应:静脉注射扎那米韦治疗的安慰剂对照试验结果
J Infect Dis. 1999 Sep;180(3):586-93. doi: 10.1086/314938.

肿瘤坏死因子α在肺上皮细胞中发挥强大的抗流感病毒作用。

Tumor necrosis factor alpha exerts powerful anti-influenza virus effects in lung epithelial cells.

作者信息

Seo Sang Heui, Webster Robert G

机构信息

Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA.

出版信息

J Virol. 2002 Feb;76(3):1071-6. doi: 10.1128/jvi.76.3.1071-1076.2002.

DOI:10.1128/jvi.76.3.1071-1076.2002
PMID:11773383
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC135862/
Abstract

Previous studies have associated influenza virus-induced expression of inflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), with influenza pathogenesis in the human respiratory tract and have suggested that alpha and beta interferons are the first cytokines recruited to counteract such infection. However, we report here that TNF-alpha has powerful anti-influenza virus activity. When infected with influenza virus, cultured porcine lung epithelial cells expressed TNF-alpha in a dose-dependent manner. Expression of TNF-alpha was induced only by replicating virus. TNF-alpha showed strong antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF-alpha was greater than that of gamma or alpha interferon. These findings suggest that TNF-alpha serves as the first line of defense against influenza virus infection in the natural host.

摘要

先前的研究已将包括肿瘤坏死因子α(TNF-α)在内的炎性细胞因子的流感病毒诱导表达与人类呼吸道的流感发病机制联系起来,并表明α和β干扰素是最早被招募来对抗此类感染的细胞因子。然而,我们在此报告TNF-α具有强大的抗流感病毒活性。当感染流感病毒时,培养的猪肺上皮细胞以剂量依赖的方式表达TNF-α。TNF-α的表达仅由复制病毒诱导。TNF-α对禽流感、猪流感和人流感病毒均表现出强大的抗病毒活性,且TNF-α的抗病毒效果大于γ或α干扰素。这些发现表明TNF-α是天然宿主中抵御流感病毒感染的第一道防线。