HSD promoted IL-17A manufacturing in mice. (A, B) Consultant and quantified stream cytometry of IL-17A-producing cells by complete lymphocytes within the spleen, peripheral blood, and mind tissues of HSD- and ND-treated mice. (C, D) Consultant and quantified stream cytometry of IL-17A-producing cells by CD3+ cells within the spleen, peripheral blood, and mind tissues of HSD- and ND-treated mice (n = 9 mice for spleen and peripheral blood; n = 3 samples for mind tissues [one sample was prepared by the brain tissues from 3 mice]; pool of two impartial experiments). Knowledge are proven because the imply ± SEM. *P The Journal of Immunology (2025). DOI: 10.1093/jimmun/vkaf019
A brand new research revealed in The Journal of Immunology discovered {that a} high-salt eating regimen (HSD) induces depression-like signs in mice by driving the manufacturing of a protein referred to as IL-17A. This protein has beforehand been recognized as a contributor to melancholy in human scientific research.
“This work supports dietary interventions, such as salt reduction, as a preventive measure for mental illness. It also paves the way for novel therapeutic strategies targeting IL-17A to treat depression,” mentioned Dr. Xiaojun Chen, a researcher at Nanjing Medical College who led the research. “We hope these findings encourage discussions on salt consumption guidelines.”
The researchers additionally recognized a kind of immune cell referred to as gamma-delta T cells (γδT cells) as an vital supply of IL-17A in HSD-fed mice, accounting for ~40% of IL-17A-producing cells. Depleting γδT cells considerably alleviated HSD-induced depressive signs, figuring out one other potential remedy technique.
Excessive-salt consumption is ubiquitous within the Western eating regimen, with quick meals typically containing 100 occasions extra salt than a home-cooked meal. HSD is already an vital public well being concern as it’s linked to cardiovascular, autoimmune, and neurodivergent ailments.
Moreover, main melancholy dysfunction can be a big public well being concern with a lifetime prevalence of 15–18% and a spot within the high 10 causes of loss of life in the US. HSD has lengthy been related to the incidence and growth of melancholy, however its function within the causation of melancholy was unclear.
On this research, mice have been fed a standard eating regimen or HSD for five weeks, a standard time-frame used to review extreme dietary salt consumption. After 5 weeks, the mice fed the HSD confirmed much less curiosity in exploring and extra inactivity in numerous eventualities in comparison with mice fed a standard eating regimen, suggesting depression-like signs in mice.
Given the already established function of IL-17A within the growth of melancholy, the analysis crew additionally investigated whether or not HSD induced IL-17A manufacturing in mice. HSD elevated IL-17A ranges within the spleen, blood, and mind, correlating with anxiety- and depression-like behaviors. Nevertheless, when mice that might not produce IL-17A have been fed an HSD, depression-like signs weren’t noticed, confirming the function of IL-17A in creating depression-like signs.
These findings corroborate epidemiological proof that HSD correlates strongly with extra extreme melancholy and research in folks demonstrating that low sodium consumption is carefully related to good temper.
The researchers hope these findings encourage additional analysis into immune-mediated mechanisms of melancholy and pave the best way for novel therapeutics focusing on IL-17A or γδT cells. Dr. Chen and their crew plan to validate these findings in people whereas additionally investigating the mechanisms by which HSD prompts γδT17 cells resulting in elevated HSD.
Extra info:
Di Lu et al, Excessive-salt eating regimen drives depression-like conduct in mice by inducing IL-17A manufacturing, The Journal of Immunology (2025). DOI: 10.1093/jimmun/vkaf019
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American Affiliation of Immunologists Inc
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Excessive-salt eating regimen linked to melancholy: Protein IL-17A performs key function in mice research (2025, March 25)
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