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牛呼吸道合胞病毒通过下调呼吸道上皮细胞表面细胞间黏附分子-1 的表达来减少多杀巴斯德菌的黏附。

Bovine Respiratory Syncytial Virus Decreased Pasteurella multocida Adherence by Downregulating the Expression of Intercellular Adhesion Molecule-1 on the Surface of Upper Respiratory Epithelial Cells.

机构信息

Graduate School of Medicine and Veterinary Medicine, University of Miyazaki, Miyazaki, Japan; Department of Veterinary Science, Faculty of Agriculture, University of Miyazaki, Miyazaki, Japan.

Graduate School of Medicine and Veterinary Medicine, University of Miyazaki, Miyazaki, Japan; Department of Veterinary Science, Faculty of Agriculture, University of Miyazaki, Miyazaki, Japan; Center for Animal Disease Control, University of Miyazaki, Miyazaki, Japan.

出版信息

Vet Microbiol. 2020 Jul;246:108748. doi: 10.1016/j.vetmic.2020.108748. Epub 2020 Jun 2.

Abstract

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.

摘要

牛呼吸道合胞体病毒(BRSV)和多杀性巴氏杆菌(PM)的协同感染可能使牛易患严重肺炎。先前,我们报道 BRSV 感染显著降低了 PM 对牛上呼吸道上皮细胞的黏附。这可能使细菌侵入下呼吸道并导致严重肺炎。为了研究 BRSV 感染是否调节牛气管上皮细胞(bTEC)的细胞表面黏附受体,我们进行了蛋白质组学和功能分析。BRSV 感染降低了 bTEC 上细胞间黏附分子-1(ICAM1)的表达。使用抗 ICAM1 抗体和针对 ICAM1 的 siRNAs 的抑制和敲低实验表明,PM 对 bTEC 的黏附依赖于 ICAM1 的表达。这些数据表明,在正常情况下,bTEC 可能在上呼吸道捕获 PM,而 BRSV 感染则逆转了这一机制。BRSV 感染破坏了 bTEC 的拟议门户功能,这可能促进细菌侵入下呼吸道并导致继发或更严重的呼吸道感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/531e/7265823/940ed05de3a2/gr1_lrg.jpg

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