EFFECT OF VITAMIN-A-DEFICIENCY ON THE IMMUNE-RESPONSE TO EPIZOOTIC DIARRHEA OF INFANT MICE (EDIM) ROTAVIRUS INFECTION IN MICE
EFFECT OF VITAMIN-A-DEFICIENCY ON THE IMMUNE-RESPONSE TO EPIZOOTIC DIARRHEA OF INFANT MICE (EDIM) ROTAVIRUS INFECTION IN MICE
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DOI：
10.1079/bjn19910106
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发表时间：
1991-05-01
影响因子：
3.6
通讯作者：
JACKSON, AA
中科院分区：
文献类型：
--
作者：
AHMED, F;JONES, DB;JACKSON, AA
本文研究了维生素A缺乏对轮状病毒致幼鼠流行性腹泻（EDIM）免疫应答的影响。病毒通过口服给药或腹腔注射给药。对于经口激发，断奶小鼠随意喂食对照或维生素A缺乏饮食。或将对照饮食与维生素A缺乏组的摄入配对喂养。第四组则是自由进食缺乏维生素A的食物。10周，然后再喂食对照饮食2周。在第77天，每只小鼠口服给予30 μ l EDIM轮状病毒，1周后处死动物并检查。迟发型超敏反应（DTH）反应苦基氯测定作为细胞介导的免疫指标。对于腹膜内激发，断奶小鼠自由采食对照饮食或维生素A缺乏饮食。或将对照饮食与维生素A缺乏组的摄入配对喂养。在第77天，每只小鼠腹膜内注射30 μ l EDIM轮状病毒，1周后测量抗体产生。在这两个实验中，维生素A缺乏组的体重、肝脏和血清维生素A水平均显著低于对照组或配对喂养组。经口给药后，维生素A缺乏动物的轮状病毒特异性血清抗体水平在统计学上显著低于对照组或配对喂养组。与对照组和成对喂养的动物相比，维生素A缺乏的小鼠也表现出受损的DTH反应。动物重新喂食维生素A一段时间后，抗体反应部分恢复。腹膜内攻击后，在任何饮食组之间的血清抗体水平中均未观察到统计学显著变化。它的结论是维生素A缺乏损害轮状病毒时，口服抗体的产生。维生素A缺乏也会损害细胞介导的免疫力。
The effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus was studied in mice. The virus was given by oral dosing or by intraperitoneal injection. For oral challenge, weanling mice were fed on either a control or vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. A fourth group was fed on the vitamin A-deficient diet ad lib. for 10 weeks and then refed the control diet for 2 weeks. On day 77, mice were each given 30-mu-l EDIM rotavirus orally and the animals were killed and examined 1 week later. The delayed-type hypersensitivity (DTH) response to picryl chloride was measured as an index of cell-mediated immunity. For intraperitoneal challenge, weanling mice were fed on either the control diet or the vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. On day 77, mice were each injected intraperitoneally with 30-mu-l EDIM rotavirus and 1 week later antibody production was measured. In both experiments the body-weight, liver and serum vitamin A levels of the vitamin A-deficient group were significantly lower than the control or pair-fed groups. Following oral dosing the serum antibody levels specific to rotavirus were statistically significantly lower in vitamin A-deficient animals than the control or pair-fed groups. Vitamin A-deficient mice also showed an impaired DTH response compared with the control and pair-fed animals. Animals refed vitamin A for a short period showed a partial restoration of the antibody response. Following intraperitoneal challenge no statistically significant changes were observed in the serum antibody levels between any of the dietary groups. It is concluded that vitamin A deficiency impaired antibody production when rotavirus was given orally. Vitamin A deficiency also impaired cell-mediated immunity.