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

•BRSV and P. multocida interaction cause severe pneumonia in cattle.•ICAM1 regulated P. multocida adherence to upper respiratory epithelial cells.•BRSV infection decreased ICAM1 expression in bovine upper respiratory tract.•Upper respiratory tract as a gateway to prevent pneumonia in lower respirato...

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Veröffentlicht in:Veterinary microbiology 2020-07, Vol.246, p.108748-108748, Article 108748
Hauptverfasser: Sudaryatma, Putu Eka, Saito, Akatsuki, Mekata, Hirohisa, Kubo, Meiko, Fahkrajang, Watcharapong, Okabayashi, Tamaki
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Sprache:eng
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Zusammenfassung:•BRSV and P. multocida interaction cause severe pneumonia in cattle.•ICAM1 regulated P. multocida adherence to upper respiratory epithelial cells.•BRSV infection decreased ICAM1 expression in bovine upper respiratory tract.•Upper respiratory tract as a gateway to prevent pneumonia in lower respiratory tract is disrupted by BRSV infection. 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.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2020.108748