Levine S, Sowinski R
J Nutr. 1980 May;110(5):891-6. doi: 10.1093/jn/110.5.891.
Previous claims that experimental allergic encephalomyelitis (EAE) was enhanced by essential fatty acid (EFA) deficiency were reinvestigated. Deficiency was induced in Lewis rats by feeding a fat-free diet starting in late gestation, at weaning or in adult life with or without a previous period of starvation. Retardation of growth, the typical dermatitis, increased water consumption and testicular atrophy gave evidence of EFA deficiency. Control rats were fed a complete diet or a fat-free diet supplemented with corn oil. EAE was induced in EFA-deficient and control rats by conventional active sensitization with neural antigen and adjuvants or by passive transfer of living lymphoid cells from sensitized nutritionally normal donors. Contrary to previous reports, EFA deficiency did not enhance EAE in any of seven experiments, and these results were supported by histological examinations. In fact, we found inhibition of clinical signs, but not histological lesions, when EFA deficiency was moderately advanced. This was accompanied by (and probably related to) thymic atrophy, possibly due to nonspecific stress. Also we found that EFA deficiency had no effect on a non-immunological model of brain inflammation that resembles EAE in the occurrence of lymphocytic infiltrates.
以往关于必需脂肪酸（EFA）缺乏会加重实验性变应性脑脊髓炎（EAE）的说法，此次重新进行了研究。通过从妊娠后期、断奶时或成年期开始喂食无脂饮食，在有或没有前期饥饿阶段的情况下，使Lewis大鼠出现必需脂肪酸缺乏。生长迟缓、典型的皮炎、饮水量增加和睾丸萎缩都表明出现了必需脂肪酸缺乏。对照大鼠喂食全价饲料或添加玉米油的无脂饲料。通过用神经抗原来进行常规主动致敏和佐剂，或通过从营养正常的致敏供体被动转移活淋巴细胞，在必需脂肪酸缺乏的大鼠和对照大鼠中诱发EAE。与以往的报道相反，在七个实验中的任何一个实验里，必需脂肪酸缺乏都没有加重EAE，组织学检查也证实了这些结果。事实上，我们发现当必需脂肪酸缺乏处于中度进展时，临床症状受到抑制，但组织学损伤并未受到抑制。这伴随着胸腺萎缩（可能与之相关），可能是由于非特异性应激所致。此外，我们发现必需脂肪酸缺乏对一种类似于EAE发生淋巴细胞浸润的非免疫性脑炎症模型没有影响。
