核因子κB和C/EBP在人呼吸道上皮细胞培养物感染呼吸道合胞病毒后对细胞间黏附分子-1调控中的重要作用。
Essential roles of NF-kappaB and C/EBP in the regulation of intercellular adhesion molecule-1 after respiratory syncytial virus infection of human respiratory epithelial cell cultures.
作者信息
Chini B A, Fiedler M A, Milligan L, Hopkins T, Stark J M
机构信息
Division of Pulmonary Medicine, Children's Hospital, Pittsburgh, Pennsylvania, USA.
出版信息
J Virol. 1998 Feb;72(2):1623-6. doi: 10.1128/JVI.72.2.1623-1626.1998.
Abstract
To determine the molecular mechanism(s) of respiratory syncytial virus (RSV)-induced intercellular adhesion molecule-1 (ICAM-1) upregulation in respiratory epithelial cells (REC; A549 cell cultures), we investigated the roles of the transcription factors NF-kappaB and C/EBP. Increases in ICAM-1 message required de novo mRNA synthesis. ICAM-1 promoter constructs (luciferase reporter gene) transfected into A549 monolayers demonstrated promoter activation following RSV infection. Activation was abolished by site-specific mutation of the NF-kappaB (-228) or C/EBP (-239) sites. These data support the critical role of the activation of NF-kappaB and C/EBP in RSV-induced ICAM-1 expression by REC.
摘要
为了确定呼吸道合胞病毒（RSV）诱导呼吸道上皮细胞（REC；A549细胞培养物）中细胞间黏附分子-1（ICAM-1）上调的分子机制，我们研究了转录因子NF-κB和C/EBP的作用。ICAM-1信使RNA的增加需要从头合成mRNA。转染到A549单层细胞中的ICAM-1启动子构建体（荧光素酶报告基因）在RSV感染后表现出启动子激活。NF-κB（-228）或C/EBP（-239）位点的位点特异性突变消除了激活。这些数据支持NF-κB和C/EBP激活在RSV诱导REC表达ICAM-1中的关键作用。
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