Elementary immunology: Na+ as a regulator of immunity

Schatz, Valentin; Neubert, Patrick; Schröder, Agnes; Binger, Katrina J.; Gebhard, Matthias; Müller, Dominik N.; Luft, Friedrich C.; Titze, Jens; Jantsch, Jonathan

doi:10.1007/s00467-016-3349-x

Cited by 61 publications

(59 citation statements)

References 102 publications

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“…Local Na + contents are known to impact homeostatic and inflammatory innate myeloid cell function (24,49). For instance, exposure of macrophages to HS¢ impaired the regulatory, antiinflammatory activity of macrophages (41), while increases in local Na + enhanced their antimicrobial activity.…”

Section: Discussionmentioning

confidence: 99%

Osteoprotective action of low-salt diet requires myeloid cell–derived NFAT5

Schröder¹,

Neubert²,

Titze³

et al. 2019

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Osteoprotective action of low-salt diet requires myeloid cell–derived NFAT5

Schröder¹,

Neubert²,

Titze³

et al. 2019

JCI Insight

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“…Sodium is involved in inflammation in hypertension and because sodium levels are in part regulated by the kidney, sodium links the kidney 104 to other systems including the integumentary system 105 .…”

Section: Sodium Hypertension and Inflammationmentioning

confidence: 99%

The systemic nature of CKD

et al. 2017

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The accurate definition and staging of chronic kidney disease (CKD) is one of the major achievements of modern nephrology. Intensive research is now being undertaken to unravel the risk factors and pathophysiologic underpinnings of this disease. In particular, the relationships between the kidney and other organs have been comprehensively investigated in experimental and clinical studies in the last two decades. Owing to technological and analytical limitations, these links have been studied with a reductionist approach focusing on two organs at a time, such as the heart and the kidney or the bone and the kidney. Here, we discuss studies that highlight the complex and systemic nature of CKD. Energy balance, innate immunity and neuroendocrine signalling are highly integrated biological phenomena. The diseased kidney disrupts such integration and generates a high-risk phenotype with a clinical profile encompassing inflammation, protein-energy wasting, altered function of the autonomic and central nervous systems and cardiopulmonary, vascular and bone diseases. A systems biology approach to CKD using omics techniques will hopefully enable in-depth study of the pathophysiology of this systemic disease, and has the potential to unravel critical pathways that can be targeted for CKD prevention and therapy.

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“…Several recent studies have shown that a high salt diet (HSD) in laboratory mice is pro-inflammatory (18). Excess NaCl in vitro was shown to enhance Th17 differentiation and activity via a p38 MAPK→NFAT5→SGK1 pathway, and that a HSD plus 1% NaCl-supplemented water exacerbates experimental autoimmune encephalitis (EAE) in mice (19, 20).…”

Section: Introductionmentioning

confidence: 99%

Dietary Salt Exacerbates Experimental Colitis

Tubbs

Liu

Rogers

et al. 2017

The Journal of Immunology

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The Western Diet – characterized by high protein, sugar, fat and low fiber intake – is widely believed to contribute to the incidence and pathogenesis of inflammatory bowel diseases (IBD). However, high sodium chloride salt content, a defining feature of processed foods, has not been considered as a possible environmental factor that might drive IBD. We set out to bridge this gap. We examined murine models of colitis on either a high salt diet (HSD) or a low salt diet (LSD). We demonstrate that a HSD exacerbates inflammatory pathology in the IL-10-deficient murine model of colitis relative to mice fed a LSD. This was correlated with enhanced expression of numerous pro-inflammatory cytokines. Surprisingly, sodium accumulated in the colons of mice on a HSD, suggesting a direct effect of salt within the colon. Similar to the IL-10-deficient model, a HSD also enhanced cytokine expression during infection by Salmonella typhimurium. This occurred in the first three day of infection, suggesting that a HSD potentiates innate immune response. Indeed, in cultured dendritic cells we found that high salt media potentiates cytokine expression downstream of TLR4 activation via p38 MAPK and SGK1. A third common colitis model, administration of dextran sodium sulfate (DSS), was hopelessly confounded by the high sodium content of the DSS. Our results raise the possibility that high dietary salt is an environmental factor that drives increased inflammation in IBD.

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Elementary immunology: Na+ as a regulator of immunity

Cited by 61 publications

References 102 publications

Osteoprotective action of low-salt diet requires myeloid cell–derived NFAT5

Osteoprotective action of low-salt diet requires myeloid cell–derived NFAT5

The systemic nature of CKD

Dietary Salt Exacerbates Experimental Colitis

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