Ketogenic diet exacerbates DSS-induced colitis through a beta-hydroxybutyrate -T. spiroformis-gd17 T cell axis in mice_Mus musculus Raw sequence reads

Ketogenic diets (KD) are widely recognized for their immunomodulatory and metabolic benefits, but their effects on inflammatory bowel disease remains controversial. We demonstrate that KD maintains homeostasis under physiological conditions but exacerbates colitis by triggering a ketogenesis-microbe-immune cascade upon mucosal injury. Specifically, KD elevates luminal beta-hydroxybutyrate (b-HB), promoting expansion of Thomasclavelia spiroformis (T. spiroformis), which activates colonic gd17 T cells via cell wall components, driving IL-17A-mediated inflammation.

生酮饮食（Ketogenic Diets，KD）因其免疫调节与代谢获益而被广泛认可，但其对炎症性肠病（Inflammatory Bowel Disease，IBD）的影响仍存在争议。本研究证实，生酮饮食在生理条件下可维持机体稳态，但在黏膜损伤时可通过触发酮生成-微生物-免疫级联反应加重结肠炎。具体而言，生酮饮食可升高肠腔β-羟基丁酸（b-HB）水平，促进螺旋形托马斯克拉维氏菌（Thomasclavelia spiroformis，T. spiroformis）的增殖，该菌可通过细胞壁成分激活结肠gd17 T细胞，进而驱动白细胞介素17A（IL-17A）介导的炎症反应。