Behera A K, Kumar M, Matsuse H, Lockey R F, Mohapatra S S
Department of Internal Medicine, University of South Florida College of Medicine, and James A. Haley VA Hospital, Tampa, FL 33612, USA.
Biochem Biophys Res Commun. 1998 Oct 29;251(3):704-9. doi: 10.1006/bbrc.1998.9537.
Respiratory syncytial virus (RSV) infection causes and exacerbates asthma, yet the mechanism by which RSV triggers asthma is poorly understood. Herein, an in vitro model of RSV infection was established using HEp-2 and BEAS-2B bronchial epithelial cell lines, and the expression of 5-lipoxygenase (5-LO), and endothelin-1 (ET-1) was examined. RSV infection increased the expression of 5-LO mRNA and protein in both cell lines, as detected by RT-PCR and western blot analysis, respectively. The levels of leukotrienes also increased in the supernatants of RSV infected cells. Furthermore, RSV infection increased the expression of ET-1 mRNA and protein following RSV infection in a time-dependent manner. It is concluded that RSV infection upregulates the expression of ET-1 and 5-LO in the epithelial cells leading to the production of leukotrienes, which may mediate the consequent exacerbation of asthma.
呼吸道合胞病毒（RSV）感染会引发并加重哮喘，但RSV引发哮喘的机制尚不清楚。在此，利用HEp-2和BEAS-2B支气管上皮细胞系建立了RSV感染的体外模型，并检测了5-脂氧合酶（5-LO）和内皮素-1（ET-1）的表达。通过RT-PCR和蛋白质印迹分析分别检测到，RSV感染增加了两种细胞系中5-LO mRNA和蛋白质的表达。RSV感染细胞的上清液中白三烯水平也有所升高。此外，RSV感染后，ET-1 mRNA和蛋白质的表达随时间呈依赖性增加。得出的结论是，RSV感染上调上皮细胞中ET-1和5-LO的表达，导致白三烯的产生，这可能介导随后哮喘的加重。
