Department of Neurology, University Hospital Erlangen, Erlangen, Germany.
Department of Neurology, Ruhr-University Bochum, Bochum, Germany.
Mult Scler. 2018 Jan;24(1):12-16. doi: 10.1177/1352458517737372.
The gut microbiome as well as dietary habits have recently been established as environmental contributors to the pathogenesis of multiple sclerosis (MS), a T-cell-mediated autoimmune disease of the central nervous system (CNS).
To summarize recent findings on the Janus-faced effects of dietary short-chain fatty acids (SCFAs) and long-chain fatty acids (LCFAs) on T-cell immunity with a special focus on the gut and the microbiome as an interface linking diet and T-cell responses during MS.
Review article.
The autoimmune basis of MS most likely stems from an imbalance between pro-inflammatory T helper cell (Th)1 and Th17 cells and anti-inflammatory or regulatory mechanisms including regulatory T cells (Treg). Hence, the rationale of currently available therapeutic interventions is to either suppress pathogenic Th1/Th17 and/or to foster Treg responses. Dietary fatty acids are often discussed for their detrimental role in MS. However, recent studies investigating saturated fatty acids in animal models of MS revealed harmful as well as beneficial effects depending on their aliphatic chain length.
Dietary SCFAs constitute interesting candidates as safe and potent add-on therapy in the immunomodulatory treatment armamentarium for relapsing-remitting MS.
肠道微生物组以及饮食习惯最近被确定为多发性硬化症(MS)发病机制的环境因素,MS 是一种中枢神经系统(CNS)的 T 细胞介导的自身免疫性疾病。
总结饮食中短链脂肪酸(SCFAs)和长链脂肪酸(LCFAs)对 T 细胞免疫的双刃剑作用的最新发现,特别关注肠道和微生物组作为连接饮食和 MS 期间 T 细胞反应的界面。
综述文章。
MS 的自身免疫基础很可能源于促炎辅助性 T 细胞(Th)1 和 Th17 细胞与抗炎或调节机制(包括调节性 T 细胞(Treg))之间的失衡。因此,目前可用的治疗干预措施的基本原理是要么抑制致病性 Th1/Th17,要么促进 Treg 反应。饮食脂肪酸通常因其在 MS 中的有害作用而被讨论。然而,最近研究发现,在 MS 的动物模型中,饱和脂肪酸的作用具有有益和有害的双重影响,这取决于其脂肪链长度。
饮食中 SCFAs 作为安全有效的辅助治疗方法,可能成为治疗复发缓解型多发性硬化症的免疫调节治疗手段之一。