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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]-1β, IL-6, IL-7, IL-8, tumor necrosis factor [TNF]-α, transforming growth factor [TGF]-β) and anti-inflammatory cytokine IL-10 in the infected group increased to varying degrees at 12 to 192 h, respectively. Furthermore, the IL-1β 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-α mRNA expression peaked at 120 h; the IL-7 mRNA expression peaked at 144 h; and the TGF-β 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-1β, IL-6, IL-7, IL-8, IL-10, TNF-α, TGF-β) 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. [ABSTRACT FROM AUTHOR]

Fasting–refeeding perturbation has been extensively used to reveal specific genes and metabolic pathways that control energy metabolism in chickens. In this study, 200 chickens were randomly assigned to 2 groups after hatching: the control group (C, fed ad libitum) and the fasting–refeeding group (T, water ad libitum). The chicks in Group T were fasted for 72 h, and then fed for another 48 h. Liver, hypothalamus, and adipose samples were collected at 0 (F0), 24 (F24), 48 (F48), and 72 h (F72) after fasting and 4 (FR4), 12 (FR12), 24 (FR24), and 48 h (FR48) after refeeding, respectively. Results showed that Group T had a significantly higher number of liver vacuoles (P < 0.05 or P < 0.01) and a significantly lower gray value of Sudan IIIstained sections (P < 0.05 or P < 0.01) than Group C at F48–FR48. In addition, compared with the Group C, fasting and refeeding reduced the expression of stearoyl CoA desaturase (SCD) mRNA (P < 0.05 or P < 0.01) in the liver and adipose tissues, the expression of glucocorticoid receptor (GR) mRNA (P < 0.05 or P < 0.01) in the liver, adipose, and hypothalamus tissues, and the expression of fatty acid synthase (FAS) mRNA (P < 0.05 or P < 0.01) in the liver at F24–FR24. Moreover, relative to those in Group C, fasting and refeeding increased the mRNA expression levels of adenosine monophosphate-activated protein kinase (AMPK) α, AMPKβ, and AMPKγ in the hypothalamus (P < 0.05 or P < 0.01) at F24–FR24. In conclusion, fasting and refeeding increased the fat content of the liver, and the expression of lipolytic genes in the hypothalamus (e.g., AMPKα, AMPKβ, and AMPKγ) but decreased the expression of fat synthesis genes in the liver (e.g., SCD, GR, and FAS), adipose (SCD and GR), and hypothalamus (GR). [ABSTRACT FROM AUTHOR]