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Life sciences · Journal article
Glia · September 25, 2026
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ABSTRACT Obesity is increasingly recognized as a chronic inflammatory condition, often driven by prolonged high‐fat diet (HFD) consumption. Beyond causing metabolic dysregulation, obesity can disrupt immune–brain communication, contributing to the development of emotional disorders. During the early stages of HFD exposure, proinflammatory cytokines such as interleukin‐1β (IL‐1β), Tumor necrosis factor‐alpha (TNF‐α), and IL‐6 are markedly elevated, but their levels typically return to baseline over time. Despite this normalization, persistent neuroinflammation and gliosis are observed, suggesting that adaptive immune mediators may play a role in chronic neuropathology. In our study using male C57BL/6 mice, 12 and 16 weeks of HFD‐induced obesity increased plasma IL‐17A levels, a key cytokine produced by CD4 + T helper 17 (Th17) cells, and upregulated IL‐17A mRNA expression in the hypothalamus. Peripheral administration of recombinant IL‐17A via intraperitoneal (i.p.) injection every 2 days for 4 weeks induced depressive and anxiety‐like behaviors, accompanied by enhanced microgliosis in emotion‐related brain regions and infiltration of CD4 + /IL‐17A + cells in the meninges. Peripheral IL‐17A administration also reduced heart rate variability (HRV), accompanied by altered HRV‐derived indices, suggesting disruption of autonomic nervous system (ANS) regulation. Systemic administration of plasma derived from mice with 12‐week HFD‐induced obesity (OB plasma) evoked depressive and anxiety‐like phenotypes, as well as ANS dysfunction. Neutralizing anti‐IL‐17A in the OB plasma effectively blocked these emotional and physiological impairments induced by OB plasma administration. Thus, our findings identify IL‐17A as a critical mediator linking metabolic dysfunction, neuroinflammation, and emotional disorders, highlighting its potential as a therapeutic target for obesity‐associated depression and anxiety.