How Salt Can Trigger Inflammation in Multiple Sclerosis

Summary: A new study reports salt could be a possible trigger for inflammation in multiple sclerosis. Researchers report cells in a high salt environment show activation of the beta catenin/Wnt signaling pathway, a pathway previously implicated in disrupting regulatory T cells and triggering inflammation.

Source: Yale.

Researchers at Yale have identified a high-salt environment as one of the contributing factors to the development of multiple sclerosis (MS).

In a new study published Oct. 29 in the journal Nature Immunology, they report just how salt can trigger the potentially disabling autoimmune disorder.

First author Tomokazu Sumida, a researcher in the lab of David Hafler, the William S. and Lois Stiles Edgerly Professor of Neurology and professor of immunobiology, and colleagues report that cells in a high-salt environment show activation of the beta-catenin/Wnt signaling pathway. This pathway, which also been implicated in the development of cancer tumors, disrupts regulatory T cells and triggers inflammation.

a salt shaker

In addition to salt, vitamin D deficiency, smoking, and obesity have been linked to development of MS, researchers say. NeuroscienceNews.com image is in the public domain.

The risk of developing MS is thought to increase by interaction between relatively common genetic variants and environmental factors. In addition to salt, vitamin D deficiency, smoking, and obesity have been linked to development of MS, researchers say.

About this neuroscience research article

Source: Bill Hathaway – Yale
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity” by Tomokazu Sumida, Matthew R. Lincoln, Chinonso M. Ukeje, Donald M. Rodriguez, Hiroshi Akazawa, Tetsuo Noda, Atsuhiko T. Naito, Issei Komuro, Margarita Dominguez-Villar & David A. Hafler in Nature Immunology. Published October 29 2018.
doi:10.1038/s41590-018-0236-6

Cite This NeuroscienceNews.com Article
Yale”How Salt Can Trigger Inflammation in Multiple Sclerosis.” NeuroscienceNews. NeuroscienceNews, 30 October 2018.
<http://neurosciencenews.com/salt-inflammation-ms-10121/>.
Yale(2018, October 30). How Salt Can Trigger Inflammation in Multiple Sclerosis. NeuroscienceNews. Retrieved October 30, 2018 from http://neurosciencenews.com/salt-inflammation-ms-10121/
Yale”How Salt Can Trigger Inflammation in Multiple Sclerosis.” http://neurosciencenews.com/salt-inflammation-ms-10121/ (accessed October 30, 2018).

Abstract

Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity

The ability to mentalize, or theory of mind (ToM), is sexually Foxp3+ regulatory T cells (Treg cells) are the central component of peripheral immune tolerance. Whereas a dysregulated Treg cytokine signature has been observed in autoimmune diseases, the regulatory mechanisms underlying pro- and anti-inflammatory cytokine production are elusive. Here, we identify an imbalance between the cytokines IFN-γ and IL-10 as a shared Treg signature present in patients with multiple sclerosis and under high-salt conditions. RNA-sequencing analysis on human Treg subpopulations revealed β-catenin as a key regulator of IFN-γ and IL-10 expression. The activated β-catenin signature was enriched in human IFN-γ+ Treg cells, as confirmed in vivo with Treg-specific β-catenin-stabilized mice exhibiting lethal autoimmunity with a dysfunctional Treg phenotype. Moreover, we identified prostaglandin E receptor 2 (PTGER2) as a regulator of IFN-γ and IL-10 production under a high-salt environment, with skewed activation of the β-catenin–SGK1–Foxo axis. Our findings reveal a novel PTGER2–β-catenin loop in Treg cells linking environmental high-salt conditions to autoimmunity.

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