Abstract
During viral respiratory infections, the innate antiviral response engages a complex network of cells and coordinates the secretion of key antiviral factors, such as cytokines, which requires high levels of regulation and communication. Extracellular vesicles (EVs) are particles released from cells that contain an array of biomolecules, including lipids, proteins, and RNAs. The contents of EVs can be influenced by viral infections and may play a role in the regulation of antiviral responses. We hypothesized that the contents of EVs released from chicken tracheal cells are influenced by viral infection and that these EVs regulate the function of other immune cells, such as macrophages. To this end, we characterized the protein profile of EVs during avian influenza virus (AIV) infection and evaluated the impact of EV stimulation on chicken macrophage functions. A total of 140 differentially expressed proteins were identified upon stimulation with various stimuli. These proteins were shown to be involved in immune responses and cell signaling pathways. In addition, we demonstrated that EVs can activate macrophages. These results suggest that EVs play a role in the induction and modulation of antiviral responses during viral respiratory infections in chickens.
Highlights
During viral respiratory infections, host innate responses aim to prevent viral entry and replication through a variety of strategies, which collectively act as the first line of defense prior to the induction of adaptive immune responses
This study provides an important overview of the contents of Extracellular vesicles (EVs) released from chicken tracheal cells under different conditions, i.e., avian influenza virus (AIV) infection, timing is of extreme importance in the context of antiviral responses, and so a key limitation of this study is that it does not evaluate the change in released EV content over time
We investigated the overall protein profile of EVs released from chicken tracheal cells in response to AIV infection and Toll-Like Receptor (TLR) ligand stimulation
Summary
Host innate responses aim to prevent viral entry and replication through a variety of strategies, which collectively act as the first line of defense prior to the induction of adaptive immune responses. Upon the infection with avian viral respiratory pathogens, such as avian influenza virus (AIV), epithelial cells become the primary target of the virus [1,2,3]. Activation of epithelial cells and macrophages following pathogen recognition leads to the recruitment of other cells of the immune system and subsequent production of interferons (IFNs), interleukins (ILs), and other pro-inflammatory cytokines. Type I IFNs, IFN-α and IFN-β, induce an antiviral state in virus-infected cells and in neighboring cells by initiating the production of IFN-stimulated genes (ISGs), which can interfere with the viral replication cycle and contribute to pathogen clearance [2,3,4]. Macrophages have other functions essential for host defense against pathogens, such as phagocytosis, secretion of antimicrobial peptides, and antigen presentation [5]
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