Fiedler M A, Wernke-Dollries K
Division of Pulmonary Medicine, Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039, USA.
J Virol. 1999 May;73(5):4502-7. doi: 10.1128/JVI.73.5.4502-4507.1999.
Respiratory syncytial virus (RSV) infection of airway epithelial cells results in persistent NF-kappaB activation and NF-kappaB-mediated interleukin-8 production. Previous studies in airway epithelial cells demonstrated that tumor necrosis factor alpha (TNF-alpha)-induced NF-kappaB activation is transient due to regulation by IkappaBalpha. However, during RSV infection, IkappaBalpha has only a partial inhibitory effect on NF-kappaB activation. Studies presented here demonstrate that neither increased IkappaBalpha production which occurs as a result of RSV-induced NF-kappaB activation nor inhibition of proteasome-mediated IkappaBalpha degradation results in a reversal of RSV-induced NF-kappaB activation. Thus, while manipulation of IkappaBalpha results in reversal of TNF-alpha-induced NF-kappaB activation, manipulation of IkappaBalpha does not result in a reversal of RSV-induced NF-kappaB activation.
呼吸道合胞病毒（RSV）感染气道上皮细胞会导致核因子κB（NF-κB）持续激活以及NF-κB介导的白细胞介素-8生成。先前对气道上皮细胞的研究表明，肿瘤坏死因子α（TNF-α）诱导的NF-κB激活是短暂的，这是由于受到IκBα的调控。然而，在RSV感染期间，IκBα对NF-κB激活仅有部分抑制作用。此处呈现的研究表明，无论是RSV诱导的NF-κB激活所导致的IκBα生成增加，还是蛋白酶体介导的IκBα降解的抑制，均不会使RSV诱导的NF-κB激活发生逆转。因此，虽然对IκBα的操控会使TNF-α诱导的NF-κB激活发生逆转，但对IκBα的操控并不会使RSV诱导的NF-κB激活发生逆转。
