RESUMO
A total of 200 one-day-old male broilers were assigned to five groups, and each group consisted of four replicates with 10 birds per replicate. Chicks were fed the basal diet with 0 (non-infected control), 0 (infected control), 10, 20, and 40 mg/kg soybean isoflavones (SI) for 42 days. At 21 days of age, chickens were inoculated with an infectious bursal dose (causing 50% morbidity) of the infectious bursal disease virus (IBDV) BC 6/85 strain by the eye-drop and nasal route (except for the non-infected group). Average daily gain (ADG) and average daily feed intake (ADFI) decreased (p < 0.05) in broilers infected with infectious bursal disease virus (IBDV) from 22 to 42 days. However, infected broilers fed 10 and 20 mg SI/kg had the maximum (p <0.05) ADG and ADFI from 1 to 42 days. Body weight (BW) increased (p < 0.05) in infected broilers fed the 10 and 20 mg SI /kg diet. The bursa weight at 7 days post-infection (dpi) was increased (p < 0.05) by the supplemental 10 mg SI/kg diet. Infected broilers showed the highest (p < 0.05) bursa lesions, with an average score of 4.0 ± 0.0, while the severity of bursa lesions was decreased (p < 0.05) at 3 dpi and 7 dpi by the supplemental 20 mg SI/kg diet. Supplemental SI at 20 mg/kg decreased (p < 0.05) the viral protein 5 (VP5) mRNA expression at 3 dpi and 7 dpi. The level of interferon gamma (IFNγ) was elevated (p < 0.05) in the infected group at 3 dpi and 7 dpi as compared with the control group, while its level was decreased (p < 0.05) by supplemental 10 mg/kg SI at 3 dpi. The level of nuclear factor κB in the bursal tissue showed the lowest value (p < 0.05) with supplemental 10 and 20 mg SI/kg diet at 7 dpi. Supplemental 10, 20, 40 mg/kg SI improved (p < 0.05) the serum total antioxidant activity (T-AOC) in infected broilers at 3 dpi. In addition, the serum level of malondialdehyde (MDA) decreased (p < 0.05) in the group fed 20 mg/kg SI at 7 dpi. In conclusion, supplemental 10~20 mg/kg SI may have a positive effect on broiler chickens infected with IBDV, probably because SI decrease the severity of bursa lesions and viral protein 5 mRNA expression, and have strong antioxidant activity.
RESUMO
OBJECTIVE: Salmonella enterica remains a major cause of food-borne disease in humans, and Salmonella Typhimurium (ST) contamination of poultry products is a worldwide problem. Since macrophages play an essential role in controlling Salmonella infection, the aim of this study was to evaluate the effect of glycyrrhizic acid (GA) on immune function of chicken HD11 macrophages. METHODS: Chicken HD11 macrophages were treated with GA (0, 12.5, 25, 50, 100, 200, 400, or 800 µg/ml) and lipopolysaccharide (LPS, 500 ng/ml) for 3, 6, 12, 24, or 48 h. Evaluated responses included phagocytosis, bacteria-killing, gene expression of cell surface molecules (cluster of differentiation 40 (CD40), CD80, CD83, and CD197) and antimicrobial effectors (inducible nitric oxide synthase (iNOS), NADPH oxidase-1 (NOX-1), interferon-γ (IFN-γ), LPS-induced tumor necrosis factor (TNF)-α factor (LITAF), interleukin-6 (IL-6), and IL-10), and production of nitric oxide (NO) and hydrogen peroxide (H2O2). RESULTS: GA increased the internalization of both fluorescein isothiocyanate (FITC)-dextran and ST by HD11 cells and markedly decreased the intracellular survival of ST. We found that the messenger RNA (mRNA) expression of cell surface molecules (CD40, CD80, CD83, and CD197) and cytokines (IFN-γ, IL-6, and IL-10) of HD11 cells was up-regulated following GA exposure. The expression of iNOS and NOX-1 was induced by GA and thereby the productions of NO and H2O2 in HD11 cells were enhanced. Notably, it was verified that nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) pathways were responsible for GA-induced synthesis of NO and IFN-γ gene expression. CONCLUSIONS: Taken together, these results suggested that GA exhibits a potent immune regulatory effect to activate chicken macrophages and enhances Salmonella-killing capacity.
