High-salt diet drives depression-like behavior in mice by inducing IL-17A production.

IF 3.4 3区 医学 Q2 IMMUNOLOGY Journal of immunology Pub Date : 2025-04-01 DOI:10.1093/jimmun/vkaf019
Di Lu, Wenjie Chen, Wenhui Sun, Chuan Wei, Xuan Xie, Na Li, Haiyan Yan, Ying Chen, Yue Wu, Zhigang Lei, Lei Xu, Jifeng Zhu, Yalin Li, Chuan Su, Wei Li, Sha Zhou, Xiaojun Chen
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Abstract

Major depression disorder is a common illness that severely limits psychosocial functioning, affects outcomes of other diseases, and diminishes the quality of life. High-salt diet (HSD) has long been closely associated with the occurrence and development of depression, but whether or how HSD causes depression remains unclear. In this study, HSD induces depression-like behavior in mice accompanied by an increase in IL-17A production. RORγt deficiency abolishes HSD-induced depression-like behavior in mice. Furthermore, γδT17 cells are identified as an important cellular source of IL-17A in mice with HSD-induced depression. Depletion of γδT cells using anti-TCRγδ antibody markedly alleviates depression-like behavior in mice with HSD. Our findings demonstrate that increased dietary salt intake facilitates the development of depression at least partially through the induction of γδT17 cells.

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高盐饮食通过诱导IL-17A的产生来驱动小鼠的抑郁样行为。
重度抑郁症是一种常见疾病,严重限制心理社会功能,影响其他疾病的结果,并降低生活质量。高盐饮食(HSD)一直被认为与抑郁症的发生发展密切相关,但高盐饮食是否或如何导致抑郁症尚不清楚。在本研究中,HSD诱导小鼠抑郁样行为,并伴有IL-17A产生的增加。RORγt缺乏可消除小鼠hsd诱导的抑郁样行为。此外,在hsd诱导的抑郁症小鼠中,γδT17细胞被鉴定为IL-17A的重要细胞来源。使用抗tcr γδ抗体消耗γδT细胞可显著减轻HSD小鼠的抑郁样行为。我们的研究结果表明,增加饮食盐摄入量至少部分通过诱导γδT17细胞促进抑郁症的发展。
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来源期刊
Journal of immunology
Journal of immunology 医学-免疫学
CiteScore
8.20
自引率
2.30%
发文量
495
审稿时长
1 months
期刊介绍: The JI publishes novel, peer-reviewed findings in all areas of experimental immunology, including innate and adaptive immunity, inflammation, host defense, clinical immunology, autoimmunity and more. Special sections include Cutting Edge articles, Brief Reviews and Pillars of Immunology. The JI is published by The American Association of Immunologists (AAI)
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