The objective of this study was to explore the mechanism by which Nephropathogenic Infectious Bronchitis Virus (NIBV) could induce chicken bursal inflammation and immune damage through the MDA5/IPS-1 signaling axis. 28 one-day old Hailan brown chicks were randomly divided into control group (Physiological saline) and diseased group (vaccination with NIBV SX9 10^-5 ELD₅₀/0.2ml). Follow up experiments were conducted on 1,7,11,13, and 18 days post-infection (dpi) of virus through observation of changes in autopsy and virus copy number detection. Histopathological sections showed an increase in interstitial fibers, a reduction in follicles and an increase in necrotic lymphocytes. The levels of IgG and IgM in the diseased group's bursa of Fabricius showed a decreasing trend. At 1dpi, the mRNA levels of the MDA5/IPS-1 signaling axis and downstream I-IFN related regulatory genes (MDA5, IPS-1, TRAF3, TBK1, IRF7, IRF3) were significantly reduced, and then significantly increased. The mRNA levels of inflammatory cytokine related regulatory genes (TRAF6, IKKβ, NF-κB P65, NF-κB, P50) downstream of the MDA5/IPS-1 signaling axis significantly increased at multiple time points. Gene expression levels of pro-inflammatory cytokines (IL-6, IL-8, TNF-α, IFN-β) in the diseased group were significantly downregulated in the early stage of the attack, and then upregulated at later time points, while protein expression levels also increased at multiple time points. NIBV infection significantly activated the MDA5/ IPS-1 signaling axis and downstreamed regulatory axis, causing the body to produce a large amount of pro-inflammatory factors, damaging the bursa of Fabricius tissue, and triggering immune disorders.

To Cite This Article: Li Z, Zhang B, Shen Y, Liu P, Shi Y, Cai G, Zheng Z, Gao X and Guo X 2025. Morphological immunological and genetic studies in the bursa of Fabricius in Nephropathogenic Infectious Bronchitis Virus -induced inflammation via the MDA5/IPS-1 signaling axis. Pak Vet J. http://dx.doi.org/10.29261/pakvetj/2025.244