Departments of Chemistry, Biochemistry, and Pharmacology, University of California, San Diego, La Jolla, CA, USA.
J Nutr. 2012 Aug;142(8):1582-9. doi: 10.3945/jn.112.157883. Epub 2012 Jun 13.
Dietary ingestion of (n-3) PUFA alters the production of eicosanoids and can suppress chronic inflammatory and autoimmune diseases. The extent of changes in eicosanoid production during an infection of mice fed a diet high in (n-3) PUFA, however, has not, to our knowledge, been reported. We fed mice a diet containing either 18% by weight soybean oil (SO) or a mixture with fish oil (FO), FO:SO (4:1 ratio), for 2 wk and then infected them with Borrelia burgdorferi. We used an MS-based lipidomics approach and quantified changes in eicosanoid production during Lyme arthritis development over 21 d. B. burgdorferi infection induced a robust production of prostanoids, mono-hydroxylated metabolites, and epoxide-containing metabolites, with 103 eicosanoids detected of the 139 monitored. In addition to temporal and compositional changes in the eicosanoid profile, dietary FO substitution increased the accumulation of 15-deoxy PGJ(2), an antiinflammatory metabolite derived from arachidonic acid. Chiral analysis of the mono-hydroxylated metabolites revealed they were generated from primarily nonenzymatic mechanisms. Although dietary FO substitution reduced the production of inflammatory (n-6) fatty acid-derived eicosanoids, no change in the host inflammatory response or development of disease was detected.
饮食摄入（n-3）多不饱和脂肪酸会改变类二十烷酸的产生，并能抑制慢性炎症和自身免疫性疾病。然而，据我们所知，在高（n-3）多不饱和脂肪酸饮食喂养的感染小鼠中，类二十烷酸产生的变化程度尚未有报道。我们用含有 18%重量大豆油（SO）或鱼油（FO）混合物的饮食（FO:SO 为 4:1 比例）喂养小鼠 2 周，然后用伯氏疏螺旋体感染它们。我们使用基于 MS 的脂质组学方法，定量分析了莱姆关节炎发展过程中类二十烷酸产生的变化，时间跨度为 21 天。B. burgdorferi 感染诱导了前列腺素、单羟基代谢物和含环氧化物代谢物的大量产生，在监测的 139 种代谢物中有 103 种被检测到。除了类二十烷酸谱的时间和组成变化外，FO 替代饮食增加了抗炎代谢物 15-脱氧 PGJ(2)的积累，该代谢物来源于花生四烯酸。单羟基代谢物的手性分析表明它们主要是通过非酶机制生成的。尽管 FO 替代饮食减少了炎症（n-6）脂肪酸衍生的类二十烷酸的产生，但未检测到宿主炎症反应或疾病发展的变化。
