Albers Ruud, Bol Marianne, Bleumink Rob, Willems Astrid A, Pieters Raymond H H
Unilever Health Institute, Utrecht, The Netherlands.
Nutrition. 2003 Nov-Dec;19(11-12):940-6. doi: 10.1016/s0899-9007(03)00178-3.
We compared the effects of supplementing with vitamins A, C, and E, selenium, and zinc on a range of innate and specific T-helper 1 (Th1) and Th2-driven adaptive immune responses.
BALB/c mice were fed semi-purified AIN93 diets and randomly assigned to receive a diet supplemented with 120 mg/kg of vitamin A, 2500 mg/kg of vitamin C, 1000 mg/kg of vitamin E, 2 mg/kg of selenium, and 500 mg/kg of zinc (n = 15/group). After 4 wk of supplementation, mice were sensitized by topical application of di-nitro-chlorobenzene (DNCB); 2 wk later mice were challenged; and 5 d later they were killed to assess the effect on a range of innate responses (phagocytic activity, oxidative burst and tumor necrosis factor-alpha), adaptive Th1-driven responses (delayed-type hypersensitivity, DNCB-specific immunoglobulin [Ig] G2a and IgG2b, and interferon-gamma [IFN-gamma]), and adaptive Th2-driven responses (DNCB-specific IgE and IgG1 and interleukin-4 [IL-4]).
Immune function was affected only in the vitamin A group. These mice gained less weight and were less capable of resolving the inflammatory response elicited during sensitization. The oxidative burst of blood cells was increased, but production of IFN-gamma and IL-4 and the ratio of IFN-gamma to IL-4 were markedly depressed. In concordance with the latter result, production of Th1-driven IgG2a antibodies was decreased, whereas Th2-driven isotypes were not affected (IgG1, IgE) and mucosal IgA was increased.
These findings confirmed that supplementary amounts of vitamin A above dietary requirements enhance inflammatory responses accompanied by decreased Th1 and increased mucosal responses. However, supplementation of these sufficiently fed, non-stressed, young adult mice with vitamins C and E, selenium, or zinc had no effect on immune function. We speculate that using this model in aged, physiologically, or nutritionally stressed mice may provide outcomes more similar to those in sensitive human populations. If so, this would improve the usefulness of the model to assess, characterize, and rank effects of foods or nutrients on a range of immune functions, including Th1/Th2 polarization.
我们比较了补充维生素A、C、E、硒和锌对一系列先天性和特定辅助性T细胞1（Th1）及辅助性T细胞2（Th2）驱动的适应性免疫反应的影响。
给BALB/c小鼠喂食半纯化的AIN93饮食，并随机分为两组，一组接受补充了120毫克/千克维生素A、2500毫克/千克维生素C、1000毫克/千克维生素E、2毫克/千克硒和500毫克/千克锌的饮食（每组n = 15）。补充4周后，通过局部涂抹二硝基氯苯（DNCB）使小鼠致敏；2周后对小鼠进行激发；5天后将其处死，以评估对一系列先天性反应（吞噬活性、氧化爆发和肿瘤坏死因子-α）、适应性Th1驱动反应（迟发型超敏反应、DNCB特异性免疫球蛋白[Ig]G2a和IgG2b以及干扰素-γ[IFN-γ]）和适应性Th2驱动反应（DNCB特异性IgE和IgG1以及白细胞介素-4[IL-4]）的影响。
仅维生素A组的免疫功能受到影响。这些小鼠体重增加较少，且在致敏过程中引发的炎症反应消退能力较弱。血细胞的氧化爆发增加，但IFN-γ和IL-4的产生以及IFN-γ与IL-4的比值明显降低。与后一结果一致，Th1驱动的IgG2a抗体产生减少，而Th2驱动的同种型（IgG1、IgE）未受影响，且黏膜IgA增加。
这些发现证实，超出饮食需求的维生素A补充量会增强炎症反应，同时Th1反应降低，黏膜反应增加。然而，给这些营养充足、无应激的年轻成年小鼠补充维生素C和E、硒或锌对免疫功能没有影响。我们推测，在年老、生理或营养应激的小鼠中使用该模型可能会得到与敏感人群更相似的结果。如果是这样，这将提高该模型在评估、表征和排列食物或营养素对一系列免疫功能（包括Th1/Th2极化）的影响方面的有用性。
