SAGE open medicine · 2026
Capsaicin attenuates high-fat diet-induced impairment of B-cell immunity.
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Yang Chengyu, Liu Zhenya, Xiong Xiaowei, Li Jiayuan, Zhao Wenjia, Liu Jian, Li Silu, Li Hui, Hang Hengjun
Аннотация
PURPOSE: Obesity contributes to immune system dysregulation, thereby increasing the risk of developing numerous diseases. Dietary capsaicin (CAP) has been demonstrated to mitigate obesity, while its impact on B cell immunity during obesity remains unexplored. This study aimed to investigate the restorative effect of CAP on B cells deficiency in obese mice, and explore the underlying mechanisms.
METHODS: C57BL/6J mice were fed a standard chow diet or a high-fat diet (HFD), and HFD-fed mice were orally administered CAP. Flow cytometry was employed to evaluate the effect of CAP on B cell function in HFD mice. RNA-seq, RT-qPCR, etc, were utilized to elucidate the underlying mechanisms.
RESULTS: CAP not only ameliorated HFD-induced metabolic abnormalities, but also reversed the HFD-associated reduction in the population of intestinal germinal center (GC) and IgA+ B cells. Consequently, CAP treatment rescued the impaired response to the T cell-dependent antigen in HFD-fed mice. Mechanistically, our results indicate that the effects of CAP are correlated with the upregulation of CXCL12/CXCR4, a pathway critically involved in GC B cell migration.
CONCLUSIONS: CAP alleviates insulin resistance and restores the impaired GC B cell in obese mice. These findings highlight a mechanism underlying the anti-obesity effect of CAP and lay a foundation for its clinical translation.
METHODS: C57BL/6J mice were fed a standard chow diet or a high-fat diet (HFD), and HFD-fed mice were orally administered CAP. Flow cytometry was employed to evaluate the effect of CAP on B cell function in HFD mice. RNA-seq, RT-qPCR, etc, were utilized to elucidate the underlying mechanisms.
RESULTS: CAP not only ameliorated HFD-induced metabolic abnormalities, but also reversed the HFD-associated reduction in the population of intestinal germinal center (GC) and IgA+ B cells. Consequently, CAP treatment rescued the impaired response to the T cell-dependent antigen in HFD-fed mice. Mechanistically, our results indicate that the effects of CAP are correlated with the upregulation of CXCL12/CXCR4, a pathway critically involved in GC B cell migration.
CONCLUSIONS: CAP alleviates insulin resistance and restores the impaired GC B cell in obese mice. These findings highlight a mechanism underlying the anti-obesity effect of CAP and lay a foundation for its clinical translation.