The synergistic infection of bovine respiratory syncytial virus (BRSV) and Pasteurella multocida (PM) may predispose cattle to develop severe pneumonia. Previously, we reported that BRSV infection significantly decreased PM adherence to the upper respiratory epithelial cells. It may allow bacteria to invade into the lower respiratory tract and lead to severe pneumonia. To investigate whether BRSV infection regulates the cell surface adherence receptor on bovine trachea epithelial cells (bTECs), we performed proteomic and functional analyses. BRSV infection decreased the expression of intercellular adhesion molecule-1 (ICAM1) on bTECs. Inhibition and knockdown experiments using anti-ICAM1 antibody and siRNAs targeting ICAM1 indicated that PM adherence to bTECs was dependent on ICAM1 expression. These data suggest that under normal conditions bTECs may capture PM in the upper respiratory tract, while BRSV infection reverses this mechanism. The proposed gateway function of bTECs is disrupted by BRSV infection that may facilitate bacterial invasion into the lower respiratory tract and lead to secondary or more severe respiratory infection.

牛呼吸道合胞病毒（BRSV）和多杀性巴斯德氏菌的协同感染（PM）可能使牛患上严重的肺炎。以前，我们报道BRSV感染显着降低PM对上呼吸道上皮细胞的粘附。它可能使细菌侵入下呼吸道并导致严重的肺炎。为了研究BRSV感染是否调节牛气管上皮细胞（bTECs）上的细胞表面粘附受体，我们进行了蛋白质组和功能分析。BRSV感染降低bTECs上的细胞间粘附分子1（ICAM1）的表达。使用抗ICAM1抗体和靶向ICAM1的siRNA进行的抑制和敲低实验表明，PM对bTEC的依附性取决于ICAM1的表达。这些数据表明，在正常情况下，bTECs可能捕获上呼吸道中的PM，而BRSV感染会逆转这种机制。