State Key Laboratory of Agrobiotechnology, Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, P. R. China.
Poult Sci. 2009 Dec;88(12):2539-48. doi: 10.3382/ps.2009-00298.
This study was conducted to determine effects of methyltestosterone on innate immunity and adaptive immunity against Salmonella Pullorum in dwarf chicks. In vivo experiment, comparisons of pathological sections, viable counts of bacteria, specific antibody levels, and subsets of T lymphocytes were set forth between chicks with or without 10(-7) M methyltestosterone treatment (2 d of age through 21 d of age) and challenged with 5 x 10(8) virulent Salmonella Pullorum (7 d of age), and in vitro experiment, phagocytic and killing abilities, reactive oxygen intermediate production, and reactive nitrogen intermediate production of monocytes-macrophages treated with high (10(-8) M/10(6) cell) or physiological (10(-14) M/10(6) cell) concentration of methyltestosterone were examined after Salmonella Pullorum infection. The results showed that (1) in vivo, administration of methyltestosterone enhanced susceptibility to Salmonella Pullorum infection and depressed cellular immunity against Salmonella Pullorum, whereas it had no effect on humoral immunity in dwarf chicks; (2) in vitro, at high concentration, methyltestosterone reduced (P < 0.05) monocytes-macrophages mediated reactive oxygen intermediate-dependent killing of Salmonella Pullorum, whereas low concentration of methyltestosterone enhanced (P < 0.05) reactive oxygen intermediate-dependent killing of Salmonella Pullorum in male dwarf chicks but not in females; and (3) although challenged with Salmonella Pullorum, phagocytic ability and monocytes-macrophages mediated reactive nitrogen intermediate-dependent killing were not affected by methyltestosterone in vitro. The results indicated that methyltestosterone affected the immune response to Salmonella Pullorum in dwarf chicks by changing monocytes-macrophages mediated reactive oxygen intermediate-dependent killing and cellular immunity, and the effects were dose-dependent; furthermore, the former 2 pathways played important roles in preventing Salmonella Pullorum infection in dwarf chicks, although the mechanism needs further study.
本研究旨在确定甲基睾丸酮对矮小鸡先天免疫和适应性免疫抗鸡白痢沙门氏菌的影响。在体内实验中，比较了未用（2 日龄至 21 日龄）和用 10(-7)M 甲基睾丸酮处理（2 日龄至 21 日龄）并攻毒 5×10(8) 强毒鸡白痢沙门氏菌（7 日龄）的雏鸡的病理切片、活菌计数、特异性抗体水平和 T 淋巴细胞亚群，在体外实验中，检测了鸡白痢沙门氏菌感染后高（10(-8)M/10(6)细胞）和生理浓度（10(-14)M/10(6)细胞）的甲基睾丸酮处理的单核细胞-巨噬细胞的吞噬和杀伤能力、活性氧中间产物的产生和活性氮中间产物的产生。结果表明：（1）体内，甲基睾丸酮给药增强了矮小鸡对鸡白痢沙门氏菌感染的易感性，抑制了对鸡白痢沙门氏菌的细胞免疫，而对体液免疫无影响；（2）体外，高浓度的甲基睾丸酮降低了（P<0.05）单核细胞-巨噬细胞介导的活性氧中间产物依赖的鸡白痢沙门氏菌杀伤能力，而低浓度的甲基睾丸酮增强了（P<0.05）雄性矮小鸡但不增强雌性矮小鸡单核细胞-巨噬细胞介导的活性氧中间产物依赖的鸡白痢沙门氏菌杀伤能力；（3）尽管受到鸡白痢沙门氏菌的攻击，体外的吞噬能力和单核细胞-巨噬细胞介导的活性氮中间产物依赖的杀伤能力不受甲基睾丸酮的影响。结果表明，甲基睾丸酮通过改变单核细胞-巨噬细胞介导的活性氧中间产物依赖的杀伤和细胞免疫来影响矮小鸡对鸡白痢沙门氏菌的免疫反应，且这种影响具有剂量依赖性；此外，前两种途径在防止矮小鸡感染鸡白痢沙门氏菌中起重要作用，尽管其机制需要进一步研究。
