Department of Neurology, Friedrich-Alexander University Erlangen, Germany.
Experimental and Clinical Research Center, A Joint Cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany; Charité-Universitätsmedizin Berlin, Germany; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Germany; Berlin Institute of Health (BIH), Berlin, Germany.
J Neuroimmunol. 2019 Apr 15;329:9-13. doi: 10.1016/j.jneuroim.2018.06.016. Epub 2018 Jun 30.
The detrimental effects of a high-salt diet on human health have received much attention in the past few years. While it has been well established that high dietary salt intake is related to cardiovascular diseases, there is growing evidence that excess salt also affects the immune system and might be considered as a risk factor in autoimmune diseases such as multiple sclerosis (MS). Several studies have implicated T helper 17 cells (Th17) in the pathogenesis of MS. We and others recently demonstrated that excessive salt enhances the differentiation of Th17 cells, inducing a highly pathogenic phenotype that aggravates experimental neuroinflammation. Moreover, a diet rich in sodium affects intestinal microbiota alongside increased intestinal Th17 cells, thus linking the detrimental effects of high salt consumption to the gut-immune axis. First human studies revealed an association of increased MS disease activity with elevated sodium chloride consumption, while more recent epidemiology studies in larger cohorts suggest no correlation between salt intake and MS. However, it is known that ordinary urinary sodium analyses and nutritional questionnaires do not necessarily correspond to the actual sodium load and more sophisticated analyses are needed. Moreover, studies revealed that sodium can temporarily be stored in the body. This review summarizes recent findings on the impact of salt on the immune system and discusses potential challenges investigating dietary salt intake as a risk factor in MS.
在过去的几年中，高盐饮食对人类健康的有害影响引起了广泛关注。虽然已经充分证实高盐饮食与心血管疾病有关，但越来越多的证据表明，过量的盐还会影响免疫系统，并可能被视为多发性硬化症（MS）等自身免疫性疾病的一个风险因素。一些研究表明，辅助性 T 细胞 17（Th17）细胞参与了 MS 的发病机制。我们和其他人最近的研究表明，过量的盐会增强 Th17 细胞的分化，诱导一种加重实验性神经炎症的高致病性表型。此外，富含钠的饮食会影响肠道微生物群，同时增加肠道 Th17 细胞，从而将高盐摄入的有害影响与肠道-免疫轴联系起来。首次人体研究表明，MS 疾病活动度增加与氯化钠摄入量增加有关，而最近在更大队列中进行的流行病学研究表明，盐摄入量与 MS 之间没有相关性。然而，众所周知，普通的尿钠分析和营养问卷并不一定与实际的钠负荷相对应，因此需要更复杂的分析。此外，研究表明，钠可以暂时储存在体内。本综述总结了最近关于盐对免疫系统影响的研究结果，并讨论了作为 MS 风险因素调查饮食盐摄入量的潜在挑战。
