Abstract
Coinfection by bovine respiratory syncytial virus (BRSV) and Pasteurella multocida (PM) frequently has been observed in cattle that develop severe pneumonia. We recently reported that BRSV infection significantly increased PM adherence to bovine lower respiratory tract epithelial cells. However, the molecular mechanisms of enhanced PM adherence are not completely understood. To investigate whether BRSV infection regulates any cellular adherence receptors on bovine bronchus- and lung-epithelial cells, we performed proteomic and functional analyses. The proteomic analysis showed that BRSV infection increased the accumulation of the platelet-activating factor receptor (PAFR) in both cell types. Molecular experiments, including specific blockade, knockdown, and overexpression of PAFR, indicated that PM adherence to these cell types depended on PAFR expression. These findings highlight the role, in cattle with severe pneumonia, of the synergistic effect of coinfection by BRSV and PM in the lower respiratory tract.
Highlights
The bovine respiratory disease complex (BRDC) is the most common health condition affecting feedlot and dairy cattle production (Gershwin et al, 2015)
We further investigated the role of platelet-activating factor receptor (PAFR) binding in Pasteurella multocida (PM) adherence to Bovine respiratory syncytial virus (BRSV)-infected bovine bronchus epithelial cells (bBECs) and bLECs by knockdown of the PAFR gene using small-interfering RNAs (siRNAs)
The results of the present study demonstrated that PAFR expression on the cell surface was upregulated by BRSV infection of bBECs and bLECs but not that of bovine trachea epithelial cells (bTECs)
Summary
The bovine respiratory disease complex (BRDC) is the most common health condition affecting feedlot and dairy cattle production (Gershwin et al, 2015). Only a few studies have examined viral induction of changes in BRECs, despite the fact that cells of this type are the portals of entry for both viruses (Goris et al, 2009; Eberle et al, 2016) and bacteria (Cozens et al, 2019) Based on these results, we suspected that BRSV infection of lower BRECs induces the production of cellular receptors and that these receptors are used as adhesion molecules by PM, increasing the risk of development of severe pneumonia. To clarify the role of BRSV infection in modulating PM adhesion to BRECs, we sought to identify the unknown surface receptor(s) whose expression is altered in cells infected by BRSV, thereby facilitating the adherence of PM
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