Department of Medical Biochemistry, Molecular Biology, and Immunology, School of Medicine, Universidad de Sevilla, Av. Dr. Fedriani 3, 41009 Seville, Spain; Department of Food & Health, Instituto de la Grasa, CSIC. Ctra. de Utrera Km. 1, 41013 Seville, Spain.
Cell Biology Unit, Instituto de la Grasa, CSIC. Ctra. de Utrera Km. 1, 41013, Seville, Spain.
J Nutr Biochem. 2020 Jan;75:108248. doi: 10.1016/j.jnutbio.2019.108248. Epub 2019 Oct 15.
Inhibiting M1 microglia phenotype while stimulating the M2 microglia has been suggested as a potential therapeutic approach for the treatment of neuroinflammatory diseases. Our hypothesis is that the type of dietary fatty acids (FAs) into human postprandial triglyceride-rich lipoproteins (TRLs) could modulate the plasticity of microglia. We isolated TRLs at the postprandial hypertriglyceridemic peak from blood samples of healthy volunteers after the ingestion of a meal rich in saturated FAs (SFAs), monounsaturated FAs (MUFAs) or MUFAs plus omega-3 long-chain polyunsaturated FAs. We observed that postprandial TRL-MUFAs enhance M2 microglia polarization, whereas postprandial TRL-SFAs made polarized microglia prone to an M1 phenotype. In addition, in contrast to dietary SFAs, dietary MUFAs primed for a reduced proinflammatory profile in the brain of mice fed with the different FA-enriched diets. Our study underlines a role of postprandial TRLs as a metabolic entity in regulating the plasticity of microglia and brings an understanding of the mechanisms by which dietary FAs are environmental factors fostering the innate immune responsiveness. These exciting findings open opportunities for developing nutraceutical strategies with olive oil as the principal source of MUFAs, notably oleic acid, to prevent development and progression of neuroinflammation-related diseases.
抑制 M1 小胶质细胞表型，同时刺激 M2 小胶质细胞，已被认为是治疗神经炎症性疾病的一种潜在治疗方法。我们的假设是，进入人体餐后富含甘油三酯的脂蛋白（TRL）的膳食脂肪酸（FAs）类型可以调节小胶质细胞的可塑性。我们在健康志愿者餐后富含饱和脂肪酸（SFAs）、单不饱和脂肪酸（MUFAs）或 MUFAs 加 omega-3 长链多不饱和脂肪酸的饮食后，从餐后高甘油三酯血症高峰期的血液样本中分离出 TRL。我们观察到，餐后 TRL-MUFAs 增强了 M2 小胶质细胞的极化，而餐后 TRL-SFAs 使极化的小胶质细胞易于表现出 M1 表型。此外，与膳食 SFAs 不同，膳食 MUFAs 为用富含不同 FA 的饮食喂养的小鼠的大脑中减少促炎特征奠定了基础。我们的研究强调了餐后 TRL 作为一种代谢实体在调节小胶质细胞可塑性方面的作用，并阐明了膳食 FAs 作为促进先天免疫反应的环境因素的作用机制。这些令人兴奋的发现为开发以橄榄油为主要来源的 MUFA 的营养策略提供了机会，特别是油酸，以预防神经炎症相关疾病的发展和进展。
