High salt intake does not exacerbate murine autoimmune thyroiditis

Kolypetri, Panayota; Randell, Edward; Vliet, Bruce N. Van; Carayanniotis, George

doi:10.1111/cei.12286

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…It has been shown that C57BL/6 substrains present behavioral [85] and genetic differences-including immune function - [86]. Moreover, other groups have shown that HSD has either no effect or even ameliorates symptoms in animal models of other inflammatory disorders [87,88]. Thus, the differences between our data and previous HSD studies, and in particular data in EAE mice, may be explained by the use of different mouse strains or by the different experimental approaches used to boost the inflammatory process, as previously discussed.…”

Section: Discussionmentioning

confidence: 99%

High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy

Heras‐Garvin¹,

Refolo²,

Reindl³

et al. 2020

J Neuroinflammation

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Aim: Pre-clinical studies in models of multiple sclerosis and other inflammatory disorders suggest that high-salt diet may induce activation of the immune system and potentiate inflammation. However, high-salt diet constitutes a common non-pharmacological intervention to treat autonomic problems in synucleinopathies such as Parkinson's disease and multiple system atrophy. Since neuroinflammation plays an important pathogenic role in these neurodegenerative disorders, we asked here whether high-salt diet may aggravate the disease phenotype in a transgenic model of multiple system atrophy. Methods: Nine-month-old PLP-hαSyn and matched wildtype mice received normal or high-salt diet for a period of 3 months. Behavioral, histological, and molecular analyses were performed to evaluate the effect of high-salt diet on motor decline, neuroinflammation, neurodegeneration, and α-synuclein accumulation in these mice. Results: Brain subregion-specific molecular and histological analyses showed no deleterious effects of high-salt diet on the level of microglial activation. Moreover, neuroinflammation-related cytokines and chemokines, T cell recruitment or astrogliosis were unaffected by high-salt diet exposure. Behavioral testing showed no effect of diet on motor decline. High-salt diet was not related to the deterioration of neurodegeneration or α-synuclein accumulation in PLP-hαSyn mice. Conclusions: Here, we demonstrate that high-salt diet does not aggravate neuroinflammation and neurodegeneration in PLP-hαSyn mice. Our findings discard a deleterious pro-neuroinflammatory effect of high-salt diet in multiple system atrophy.

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Section: Discussionmentioning

confidence: 99%

High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy

Heras‐Garvin¹,

Refolo²,

Reindl³

et al. 2020

J Neuroinflammation

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“…(a) as a promoter of local renal, cutaneous and/or systemic autoimmune response through imbalances of saltwater balances [8,20,21]; (b) as a precipitating factor of glomerular injury, due to its pivotal role in the maintenance of podocytes anatomy [12].…”

Section: Discussionmentioning

confidence: 99%

Beta-adducin and sodium–calcium exchanger 1 gene variants are associated with systemic lupus erythematosus and lupus nephritis

et al. 2015

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Genetic research in systemic lupus erythematosus (SLE) is rapidly developing, and numerous sets of genes are being associated with specific clinical subphenotypes in the setting of SLE. On the other hand, basic science studies are revealing strong connections between salt-water balance and inflammation. The aim of this study was to evaluate whether variants of genes known to influence the individual susceptibility to hypertension also influence the renal function in a cohort of SLE patients with and without lupus nephritis (LN). This study is a case-control study with candidate gene approach. A total of 111 patients with SLE (50 with SLE without nephritis, 55 with LN and 6 with simple urinary sediment abnormalities) and 62 healthy controls (HC) were genotyped for NCX1 rs11893826 (NCX1a) and rs434082 (NCX1b) and ADD2 rs4984 SNPs. Patients with ADD2 CT genotype were protected from LN and skin involvement; ADD2 CC | NCX1a AA/AG genotypes were associated with the presence of anti-cardiolipin antibodies; NCX1a AA genotype was slightly more frequent in lupus patients than in HC and associated with relapse risk and higher creatinine in patients with LN. NCX1b GG patients with LN had increased chances to reach complete remission. NCX1b GG | NCX1a GG genotype is associated with joint involvement. ADD2 and NCX1 variants influence the risk and the clinical features of SLE and LN, highlighting their potential role in regulating systemic inflammation and/or the local response to immune-mediated injury.

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“…Twenty-one female NOD mice with approximately 8-week of age, weighing 21 24 g were obtained from Beijing HFK Bioscience (SCXK 2014-0004) and randomly divided into control (n = 10) or HT groups (n = 11). In this study, we only utilized female mice given that HT is more prevalent in women than in men [2], and given that female mice have primarily been used in prior preclinical studies of HT [29][30][31]. Mice were housed in groups of 3-4 at 23 ± 2℃, 55 ± 5%, humidity and a 12-h light/dark cycle with free access to standard food and water.…”

Section: Animals and Study Designmentioning

confidence: 99%

Synaptic Loss in a Mouse Model of Euthyroid Hashimoto’s Thyroiditis: Possible Involvement of the Microglia

Wang¹,

Cai²,

Ma³

et al. 2021

Preprint

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Background: Hashimoto’s thyroiditis (HT) is an autoimmune illness that renders individuals vulnerable to neuropsychopathology even in the euthyroid state, the mechanisms involved remain unclear. We hypothesized that activated microglia might disrupt synapses, resulting in cognitive disturbance in the context of euthyroid HT, and designed the present study to test this hypothesis. Methods: Experimental HT model was induced by immunizing NOD mice with thyroglobulin and adjuvant twice. Morris Water Maze was measured to determine mice spatial learning and memory. The synaptic parameters such as the synaptic density, synaptic ultrastructure and synaptic-markers (SYN and PSD95) as well as the interactions of microglia with synapses were also determined. Results: HT mice had poorer performance in Morris Water Maze than controls. Concurrently, HT resulted in a significant reduction in synapse density and ultrastructure damage, along with decreased synaptic puncta visualized by immunostaining with synaptophysin and PSD-95. In parallel, frontal activated microglia in euthyroid HT mice showed increased engulfment of PSD95 and EM revealed that the synaptic structures were visible within the microglia. These functional alterations in microglia corresponded to structural increases in their attachment to neuronal perikarya and a reduction in presynaptic terminals covering the neurons.Conclusion: Our results provide initial evidence that HT can induce synaptic loss in the euthyroid state with deficits might be attributable to activated microglia, which may underlie the deleterious effects of HT on spatial learning and memory.

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High salt intake does not exacerbate murine autoimmune thyroiditis

Cited by 7 publications

References 30 publications

High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy

High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy

Beta-adducin and sodium–calcium exchanger 1 gene variants are associated with systemic lupus erythematosus and lupus nephritis

Synaptic Loss in a Mouse Model of Euthyroid Hashimoto’s Thyroiditis: Possible Involvement of the Microglia

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