ArticleAnimal bioscience2024
In vitro analysis of antiviral immune response against avian influenza virus in chicken tracheal epithelial cells.
Article in Animal bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Future-ready antimicrobials: harnessing organic acids to override CaMicrobiology (Reading, England) · 2026Article
- Host genetics, lung T-cell immunity, and laying activity determine the disease outcome in avian influenza virus-infected chickens.Veterinary research · 2026Article
- Advances and prospects of mucosal vaccination in the prevention and control of avian influenza.Frontiers in immunology · 2026Review
- Comparative Evaluation of Three Rapid Influenza Diagnostic Tests for Detection of Influenza A and B Viruses Using RT-PCR as Reference Method.Journal of medical virology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
objectiveAvian influenza virus (AIV) infections first affect the respiratory tract of chickens. The epithelial cells activate the host immune system, which leads to the induction of immune-related genes and the production of antiviral molecules against external environmental pathogens. In this study, we used chicken tracheal epithelial cells (TECs) in vitro model to investigate the immune response of the chicken respiratory tract against avian respiratory virus infections.
methodsEighteen-day-old embryonic chicken eggs were used to culture the primary chicken TECs. Reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry (ICC) analysis of epithelial cell-specific gene makers were performed to confirm the characteristics, morphology, and growth pattern of primary cultured chicken TECs. Moreover, to investigate the cellular immune response to AIV infection or polyinosinic-polycytidylic acid (poly [I:C]) treatment, the TECs were infected with the H5N1 virus or poly (I:C). Then, immune responses were validated by RT-qPCR and western blotting.
resultsThe TECs exhibited polygonal morphology and formed colony-type cell clusters. The RT-qPCR results showed that H5N1 infection induced a significant expression of antiviral genes in TECs. We found that TECs treated with poly (I:C) and exposed to AIV infection-mediated activation of signaling pathways, leading to the production of antiviral molecules (e.g., pro-inflammatory cytokines and chemokines), were damaged due to the loss of junction proteins. We observed the activation of the nuclear factor kappa B and mitogen-activated protein kinase (MAPK) pathways, which are involved in inflammatory response by modulating the release of pro-inflammatory cytokines and chemokines in TECs treated with poly (I:C) and pathway inhibitors. Furthermore, our findings indicated that poly (I:C) treatment compromises the epithelial cell barrier by affecting junction proteins in the cell membrane.
conclusionOur study highlights the utility of in vitro TEC models for unraveling the mechanisms of viral infection and understanding host immune responses in the chicken respiratory tract.
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