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High salt intake does not exacerbate murine autoimmune thyroiditis
Author(s) -
Kolypetri P.,
Randell E.,
Van Vliet B. N.,
Carayanniotis G.
Publication year - 2014
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12286
Subject(s) - autoimmune thyroiditis , medicine , thyroiditis , endocrinology , thyroglobulin , autoimmune disease , immunology , experimental autoimmune encephalomyelitis , nod , autoimmunity , antibody , thyroid , immune system , diabetes mellitus
Summary 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 ( T g) and EAT in CBA/J mice challenged with the T g 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 T g‐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.

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