Division of Endocrinology, Faculty of Medicine, Memorial University of Newfoundland, St John's, NL, Canada; Division of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St John's, NL, Canada.
Clin Exp Immunol. 2014 Jun;176(3):336-40. doi: 10.1111/cei.12286.
Recent studies have shown that high salt (HS) intake exacerbates experimental autoimmune encephalomyelitis and have raised the possibility that a HS diet may comprise a risk factor for autoimmune diseases in general. In this report, we have examined whether a HS diet regimen could exacerbate murine autoimmune thyroiditis, including spontaneous autoimmune thyroiditis (SAT) in non-obese diabetic (NOD.H2(h4)) mice, experimental autoimmune thyroiditis (EAT) in C57BL/6J mice challenged with thyroglobulin (Tg) and EAT in CBA/J mice challenged with the Tg peptide (2549-2560). The physiological impact of HS intake was confirmed by enhanced water consumption and suppressed aldosterone levels in all strains. However, the HS treatment failed to significantly affect the incidence and severity of SAT or EAT or Tg-specific immunoglobulin (Ig)G levels, relative to control mice maintained on a normal salt diet. In three experimental models, these data demonstrate that HS intake does not exacerbate autoimmune thyroiditis, indicating that a HS diet is not a risk factor for all autoimmune diseases.
最近的研究表明,高盐(HS)摄入会加重实验性自身免疫性脑脊髓炎,并提出高盐饮食可能是一般自身免疫性疾病的一个风险因素。在本报告中,我们研究了高盐饮食方案是否会加重实验性自身免疫性甲状腺炎,包括非肥胖型糖尿病(NOD.H2(h4))小鼠的自发性自身免疫性甲状腺炎(SAT)、Tg 刺激的 C57BL/6J 小鼠的实验性自身免疫性甲状腺炎(EAT)以及 Tg 肽(2549-2560)刺激的 CBA/J 小鼠的 EAT。所有品系的高盐摄入均通过增加水的摄取量和降低醛固酮水平来证实其生理影响。然而,与维持正常盐饮食的对照小鼠相比,高盐处理并没有显著影响 SAT 或 EAT 的发生率和严重程度,也没有显著影响 Tg 特异性免疫球蛋白(IgG)水平。在三个实验模型中,这些数据表明,高盐摄入不会加重自身免疫性甲状腺炎,这表明高盐饮食不是所有自身免疫性疾病的一个风险因素。