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Nutrients. 2019 May 5;11(5):1013. doi: 10.3390/nu11051013.
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Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity.氯化钠促进促炎型巨噬细胞极化,从而加重中枢神经系统自身免疫。
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High dietary salt intake activates inflammatory cascades via Th17 immune cells: impact on health and diseases.高盐饮食通过Th17免疫细胞激活炎症级联反应:对健康和疾病的影响。
Arch Med Sci. 2020 Jun 15;18(2):459-465. doi: 10.5114/aoms.2020.96344. eCollection 2022.

本文引用的文献

1
Negligible Effect of Sodium Chloride on the Development and Function of TGF-β-Induced CD4 Foxp3 Regulatory T Cells.氯化钠对 TGF-β诱导的 CD4 Foxp3 调节性 T 细胞的发育和功能影响可忽略不计。
Cell Rep. 2019 Feb 12;26(7):1869-1879.e3. doi: 10.1016/j.celrep.2019.01.066.
2
Sodium Chloride Aggravates Arthritis via Th17 Polarization.氯化钠通过Th17极化加重关节炎。
Yonsei Med J. 2019 Jan;60(1):88-97. doi: 10.3349/ymj.2019.60.1.88.
3
High salt diet ameliorates functional, electrophysiological and histological characteristics of murine spontaneous autoimmune polyneuropathy.高盐饮食可改善自发性自身免疫性多神经病的功能、电生理和组织学特征。
Neurobiol Dis. 2019 Apr;124:240-247. doi: 10.1016/j.nbd.2018.11.017. Epub 2018 Nov 22.
4
Analysis of Sodium Chloride Intake and Treg/Th17 Lymphocytes in Healthy Individuals and Patients with Rheumatoid Arthritis or Systemic Lupus Erythematosus.健康个体与类风湿关节炎或系统性红斑狼疮患者的氯化钠摄入量与 Treg/Th17 淋巴细胞分析。
J Immunol Res. 2018 Jul 9;2018:9627806. doi: 10.1155/2018/9627806. eCollection 2018.
5
Increased salt exposure affects both lymphoid and myeloid effector functions, influencing innate-associated disease but not T-cell-associated autoimmunity.增加盐暴露会影响淋巴样和髓样效应功能,影响与先天免疫相关的疾病,但不影响与T细胞相关的自身免疫。
Immunology. 2018 Mar 7;154(4):683-94. doi: 10.1111/imm.12923.
6
SGK1 Governs the Reciprocal Development of Th17 and Regulatory T Cells.SGK1 调控 Th17 与调节性 T 细胞的协同发育。
Cell Rep. 2018 Jan 16;22(3):653-665. doi: 10.1016/j.celrep.2017.12.068.
7
Elevated sodium chloride drives type I interferon signaling in macrophages and increases antiviral resistance.高浓度氯化钠可驱动巨噬细胞中的 I 型干扰素信号转导,并增强抗病毒能力。
J Biol Chem. 2018 Jan 19;293(3):1030-1039. doi: 10.1074/jbc.M117.805093. Epub 2017 Dec 4.
8
Vitamin D status in spondyloarthritis: results of the ASAS-COMOSPA international study.脊柱关节炎患者的维生素 D 状况:ASAS-COMOSPA 国际研究结果。
Clin Exp Rheumatol. 2018 Mar-Apr;36(2):210-214. Epub 2017 Nov 16.
9
Salt-responsive gut commensal modulates T17 axis and disease.盐反应性肠道共生菌调节T17轴与疾病。
Nature. 2017 Nov 30;551(7682):585-589. doi: 10.1038/nature24628. Epub 2017 Nov 15.
10
Dendritic Cell Amiloride-Sensitive Channels Mediate Sodium-Induced Inflammation and Hypertension.树突状细胞阿米洛利敏感通道介导钠诱导的炎症和高血压。
Cell Rep. 2017 Oct 24;21(4):1009-1020. doi: 10.1016/j.celrep.2017.10.002.

饮食习惯引发自身免疫性疾病的复杂发病机制:来自实验和临床研究的盐的新作用。

Dietary Habits Bursting into the Complex Pathogenesis of Autoimmune Diseases: The Emerging Role of Salt from Experimental and Clinical Studies.

机构信息

Department of Internal Medicine and Medical Specialties, Rheumatology, Sapienza University of Rome, Rome 00185, Italy.

出版信息

Nutrients. 2019 May 5;11(5):1013. doi: 10.3390/nu11051013.

DOI:10.3390/nu11051013
PMID:31060286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6566149/
Abstract

The incidence and prevalence of autoimmune diseases have increased in Western countries over the last years. The pathogenesis of these disorders is multifactorial, with a combination of genetic and environmental factors involved. Since the epidemiological changes cannot be related to genetic background, which did not change significantly in that time, the role of environmental factors has been reconsidered. Among these, dietary habits, and especially an excessive salt, typical of processed foods, has been implicated in the development of autoimmune diseases. In this review, we summarize current evidence, deriving both from experimental models and clinical studies, on the capability of excessive salt intake to exacerbate proinflammatory responses affecting the pathogenesis of immune-mediated diseases. Data on several diseases are presented, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and Crohn's disease, with many of them supporting a proinflammatory effect of salt. Likewise, a hypertonic microenvironment showed similar effects in experimental models both in vivo and in vitro. However, murine models of spontaneous autoimmune polyneuropathy exposed to high salt diet suggest opposite outcomes. These results dictate the need to further analyse the role of cooking salt in the treatment and prevention of autoimmune diseases, trying to shape a fine tuning between the possible advantages of a restricted salt intake and the changes in circulating metabolites, mediators, and hormones which come along salt consumption and could in turn influence autoimmunity.

摘要

近年来,自身免疫性疾病在西方国家的发病率和患病率有所上升。这些疾病的发病机制是多因素的,涉及遗传和环境因素的结合。由于流行病学的变化不能与遗传背景相关,而遗传背景在那段时间并没有显著改变,因此环境因素的作用再次受到了关注。在这些因素中,饮食习惯,尤其是加工食品中过量的盐,被认为与自身免疫性疾病的发展有关。在这篇综述中,我们总结了目前来自实验模型和临床研究的证据,表明过量盐摄入可加重影响免疫介导性疾病发病机制的促炎反应。介绍了几种疾病的数据,包括类风湿关节炎、系统性红斑狼疮、多发性硬化症和克罗恩病,其中许多疾病都支持盐的促炎作用。同样,高渗微环境在体内和体外的实验模型中也表现出类似的作用。然而,暴露于高盐饮食的自发性自身免疫性多发性神经病的小鼠模型表明了相反的结果。这些结果表明,需要进一步分析烹饪盐在自身免疫性疾病的治疗和预防中的作用,试图在限制盐摄入的可能优势和盐消费带来的循环代谢物、介质和激素的变化之间取得平衡,这些变化反过来又可能影响自身免疫。