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Analysis of chicken macrophage functions and gene expressions following infectious bronchitis virus M41 infection

Xiaoqi Sun, Zheng Wang, Changhao Shao, Jia Yu, Haoyun Liu, Huijie Chen, Lu Li, Xiurong Wang, Yudong Ren, Xiaodan Huang, Ruili Zhang, Guangxing Li
BMC veterinary research 2021 v.52 no.1 pp. 14
Infectious bronchitis virus, adaptive immunity, apoptosis, autophagy, blood, cell lines, cell viability, chickens, genes, inflammation, interleukin-10, interleukin-6, macrophages, morbidity, mortality, pathogens, phagocytosis, veterinary medicine, virus replication
Infectious bronchitis virus (IBV) is a pathogenic coronavirus with high morbidity and mortality in chicken breeding. Macrophages with normal biofunctions are essential for host immune responses. In this study, the HD11 chicken macrophage cell line and chicken peripheral blood mononuclear cell-derived macrophages (PBMCs-Mφ) were infected with IBV at multiplicity of infection (MOI) of 10. The dynamic changes of their biofunctions, including cell viability, pathogen elimination function, phagocytic ability, and gene expressions of related proteins/mediators in innate and acquired immunity, inflammation, autophagy and apoptosis were analyzed. Results showed that IBV infection decreased chicken macrophage viability and phagocytic ability, and increased pathogen elimination function. Moreover, IBV augmented the gene expressions of most related proteins in macrophages involved in multiple host bioprocesses, and the dynamic changes of gene expressions had a close relationship with virus replication. Among them, MHCII, Fc receptor, TLR3, IFN-α, CCL4, MIF, IL-1β, IL-6, and iNOS showed significantly higher expressions in IBV-infected cells. However, TLR7, MyD88, MDA5, IFN-γ, MHCII, Fc receptor, MARCO, CD36, MIF, XCL1, CXCL12, TNF-α, iNOS, and IL-10 showed early decreased expressions. Overall, chicken macrophages play an important role in host innate and acquired immune responses to resist IBV infection, despite early damage or suppression. Moreover, the IBV-induced autophagy and apoptosis might participate in the virus-host cell interaction which is attributed to the biological process.