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膳食脂质对小鼠致敏模型免疫功能的影响。

Effects of dietary lipids on immune function in a murine sensitisation model.

作者信息

Albers Ruud, Bol Marianne, Bleumink Rob, Willems Astrid, Blonk Cor, Pieters Raymond

机构信息

Unilever Health Institute, P.O. Box 114, 3130 AC Vlaardingen, The Netherlands.

出版信息

Br J Nutr. 2002 Sep;88(3):291-9. doi: 10.1079/BJN2002614.

Abstract

We have tested the effect of dietary fatty acids on aspects of innate and specific adaptive T helper (Th) 1- and Th2-driven immune responses in a murine sensitisation model using dinitrochlorobenzene as sensitiser. Six groups of fifteen BALB/c mice were fed diets containing 30 % fat (by energy) for 8 weeks. Diets were rich in saturated fatty acids, n-6 polyunsaturated fatty acid (PUFA), or n-3 PUFA, each at a sufficient (11, 35 and 68 mg/kg) and a supplemented vitamin E level (1028, 1031 and 1030 mg/kg respectively). Feeding n-6 PUFA marginally decreased % phagocytosing cells at the low vitamin E level, but had no other effects on immune function. The n-3 PUFA diets decreased production of prostaglandin E2 while increasing oxidative burst and tumour necrosis factor alpha production. In addition adaptive Th1-driven responses (immunoglobulin, Ig)G2a, IgG2b, interferon-gamma:interleukin 4) were decreased, whereas Th2-driven and mucosal immune responses were increased (IgE) or unaffected (IgG1, IgA). Combination with high levels of alpha-tocopherol did not affect the reduced prostaglandin E2 production, augmented the increase of tumour necrosis factor alpha production and tended to ameliorate the selective suppressive effects of n-3 PUFA on certain Th1-driven effects (interferon-gamma:interleukin 4 ratio and IgG2a levels). We conclude that the sensitisation model appears useful for application in nutrition research. It allows a broad assessment of the effects of dietary intervention on various aspects of immune responsiveness, and as such provides a valuable model to assess, characterise and rank effects of foods and/or nutrients on a range of immune functions, including Th1-Th2 polarisation.

摘要

我们在以二硝基氯苯作为致敏剂的小鼠致敏模型中,测试了膳食脂肪酸对固有免疫以及特定适应性T辅助(Th)1和Th2驱动的免疫反应各方面的影响。将六组每组15只BALB/c小鼠喂食含30%脂肪(能量占比)的饮食8周。饮食富含饱和脂肪酸、n-6多不饱和脂肪酸(PUFA)或n-3 PUFA,每种脂肪酸均设置了充足水平(分别为11、35和68毫克/千克)以及补充了维生素E的水平(分别为1028、1031和1030毫克/千克)。在低维生素E水平下,喂食n-6 PUFA会使吞噬细胞百分比略有下降,但对免疫功能无其他影响。n-3 PUFA饮食可降低前列腺素E2的产生,同时增加氧化爆发和肿瘤坏死因子α的产生。此外,适应性Th1驱动的反应(免疫球蛋白IgG2a、IgG2b、干扰素-γ:白细胞介素4)减少,而Th2驱动的和黏膜免疫反应增加(IgE)或未受影响(IgG1、IgA)。与高水平的α-生育酚联合使用并不影响前列腺素E2产生的减少,增强了肿瘤坏死因子α产生的增加,并倾向于改善n-3 PUFA对某些Th1驱动效应(干扰素-γ:白细胞介素4比值和IgG2a水平)的选择性抑制作用。我们得出结论,该致敏模型似乎适用于营养研究。它允许广泛评估膳食干预对免疫反应性各个方面的影响,因此为评估、表征和排序食物和/或营养素对一系列免疫功能(包括Th1-Th2极化)的影响提供了一个有价值的模型。

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