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Lewis大鼠的必需脂肪酸缺乏、前列腺素合成与体液免疫

Essential fatty acid deficiency, prostaglandin synthesis and humoral immunity in Lewis rats.

作者信息

Boissonneault G A, Johnston P V

出版信息

J Nutr. 1983 Jun;113(6):1187-94. doi: 10.1093/jn/113.6.1187.

Abstract

Essential fatty acid (EFA) deficiency is known to alter the immune response in several experimental systems. To further evaluate the effects of EFAs on immunity Lewis rats were fed diets either adequate or deficient in EFAs for 70-80 days. EFA-adequate rats responded to an i.v. injection of 5 X 10(8) sheep erythrocytes with a sharp, short-lived rise in splenic levels of PGE and PGF within 2 minutes after injection. EFA deficiency resulted in a diminution of this PG response. PG production in liver homogenates was also depressed in EFA-deficient liver. An i.v. injection of sheep erythrocytes resulted in a humoral response against this antigen, measured as hemolytic plaque-forming cells in the spleen. EFA deficiency, as well as pretreatment of EFA-adequate rats with indomethacin, an inhibitor of PG synthesis, resulted in a stimulation of the plaque-forming cell response over that observed in control, EFA-adequate rats. The alterations in immune response resulting from changes in PG synthetic capacity may be important in the etiology of certain immunodeficiency syndromes such as the lupus-erythematosus-like autoimmune disease in NZB/W mice.

摘要

已知必需脂肪酸(EFA)缺乏会在多个实验系统中改变免疫反应。为了进一步评估必需脂肪酸对免疫的影响,给Lewis大鼠喂食富含或缺乏必需脂肪酸的饲料70 - 80天。摄入充足必需脂肪酸的大鼠在静脉注射5×10⁸个绵羊红细胞后,注射后2分钟内脾脏中PGE和PGF水平急剧短暂升高。必需脂肪酸缺乏导致这种PG反应减弱。缺乏必需脂肪酸的肝脏中肝匀浆的PG生成也受到抑制。静脉注射绵羊红细胞会引发针对该抗原的体液反应,以脾脏中溶血空斑形成细胞来衡量。必需脂肪酸缺乏以及用PG合成抑制剂吲哚美辛预处理摄入充足必需脂肪酸的大鼠,导致空斑形成细胞反应比对照的、摄入充足必需脂肪酸的大鼠有所增强。PG合成能力变化引起的免疫反应改变可能在某些免疫缺陷综合征的病因学中起重要作用,如NZB/W小鼠中的红斑狼疮样自身免疫性疾病。

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