Differential expression of pro-inflammatory and anti-inflammatory genes of layer chicken bursa after experimental infection with infectious bursal disease virus

Infectious bursal disease (IBD) is one of the most prevalent infectious diseases caused by IBD virus (IBDV), which results in bursal necrosis and immunosuppression that cause severe damage to the immune system in chickens. Cytokines are important mediators and regulators of both types of host responses. In the present study, layer chickens were artificially challenged with IBDV, and the differential expression of inflammatory genes was explored by using quantitative real-time PCR, which offered basic data for further study of IBDV pathogenesis. Data showed that after IBDV infection, the virus load in the bursa of Fabricius (BF) peaked at 96 h and then gradually decreased. Compared with those of the negative-infected group, the mRNA expression levels of pro-inflammatory cytokines (interleukin [IL]-1 beta, IL-6, IL-7, IL-8, tumor necrosis factor [TNF]-alpha, transforming growth factor [TGF]-beta) and anti-inflammatory cytokine IL-10 in the infected group increased to varying degrees at 12 to 192 h, respectively. Furthermore, the IL-1 beta mRNA expression peaked at 48 h; the mRNA transcript levels of IL-6, IL-8, and IL-10 were the highest at 96 h; TNF-alpha mRNA expression peaked at 120 h; the IL-7 mRNA expression peaked at 144 h; and the TGF-beta mRNA transcript level was the highest at 192 h. Taken together, these observations indicated that along with the change pattern of IBDV proliferation in BF, the mRNA expression of cytokines (IL-1 beta, IL-6, IL-7, IL-8, IL-10, TNF-alpha, TGF-beta) obviously increased, and the kinetics of each of these cytokines was different. The kinetics of IL-6/IL-10 mRNA expression ratio was significantly positively correlated with that of the virus load. These results suggest that IBDV infection seriously interferes with the natural immune response mediated by inflammatory cytokines in chickens.