Food Science, Department of Chemical and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden.
Clin Exp Immunol. 2010 Jun;160(3):411-9. doi: 10.1111/j.1365-2249.2010.04107.x. Epub 2010 Feb 10.
Studies have shown that atopic individuals have decreased serum levels of n-3 fatty acids. Indicating these compounds may have a protective effect against allergic reaction and/or are consumed during inflammation. This study investigated whether fish (n-3) or sunflower (n-6) oil supplementation affected T helper type 1 (Th1)- and Th2-mediated hypersensitivity in the skin and airways, respectively, and whether the fatty acid serum profile changed during the inflammatory response. Mice were fed regular chow, chow + 10% fish oil or chow + 10% sunflower oil. Mice were immunized with ovalbumin (OVA) resolved in Th1 or Th2 adjuvant. For Th1 hypersensitivity, mice were challenged with OVA in the footpad. Footpad swelling, OVA-induced lymphocyte proliferation and cytokine production in the draining lymph node were evaluated. In the airway hypersensitivity model (Th2), mice were challenged intranasally with OVA and the resulting serum immunoglobulin (Ig)E and eosinophilic lung infiltration were measured. In the Th1 model, OVA-specific T cells proliferated less and produced less interferon (IFN)-gamma, tumour necrosis factor (TNF) and interleukin (IL)-6 in fish oil-fed mice versus controls. Footpad swelling was reduced marginally. In contrast, mice fed fish oil in the Th2 model produced more OVA-specific IgE and had slightly higher proportions of eosinophils in lung infiltrate. A significant fall in serum levels of long-chain n-3 fatty acids accompanied challenge and Th2-mediated inflammation in Th2 model. Fish oil supplementation affects Th1 and Th2 immune responses conversely; significant consumption of n-3 fatty acids occurs during Th2-driven inflammation. The latter observation may explain the association between Th2-mediated inflammation and low serum levels of n-3 fatty acids.
研究表明,特应性个体的血清 n-3 脂肪酸水平降低。这表明这些化合物可能对过敏反应具有保护作用,或者在炎症期间被消耗。本研究旨在探讨鱼油(n-3)或葵花籽油(n-6)补充是否分别影响皮肤和气道中的 T 辅助型 1(Th1)和 Th2 介导的过敏反应,以及在炎症反应过程中脂肪酸血清谱是否发生变化。小鼠分别喂食常规饲料、含 10%鱼油的饲料或含 10%葵花籽油的饲料。用卵清蛋白(OVA)在 Th1 或 Th2 佐剂中免疫小鼠。对于 Th1 过敏反应,用 OVA 对小鼠的足底进行攻击。评估足垫肿胀、OVA 诱导的引流淋巴结淋巴细胞增殖和细胞因子产生。在气道过敏反应模型(Th2)中,用 OVA 对小鼠进行鼻内攻击,测量由此产生的血清免疫球蛋白(Ig)E 和嗜酸性粒细胞肺浸润。在 Th1 模型中,与对照组相比,鱼油喂养的小鼠 OVA 特异性 T 细胞增殖减少,干扰素(IFN)-γ、肿瘤坏死因子(TNF)和白细胞介素(IL)-6 产生减少。足垫肿胀略有减少。相比之下,在 Th2 模型中,喂食鱼油的小鼠产生更多的 OVA 特异性 IgE,并且肺浸润中嗜酸性粒细胞的比例略高。在 Th2 模型中,长链 n-3 脂肪酸的血清水平在挑战和 Th2 介导的炎症时显著下降。鱼油补充剂对 Th1 和 Th2 免疫反应的影响相反;在 Th2 驱动的炎症期间,大量消耗 n-3 脂肪酸。后一种观察结果可能解释了 Th2 介导的炎症与 n-3 脂肪酸血清水平降低之间的关联。