果糖摄入驱动的糖解-ROS-EGFR轴特别促进Th17细胞的生成和致病性
Xiaoyu Liu1,2, Wenhao Hu1,2, Jie Sun1,2
1Department of Urology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Nature communications
|November 23, 2025
概括
高果糖摄入量会通过促进致病性T辅助17 (Th17) 细胞恶化大肠炎和EAE等炎症性疾病. N-乙囊 (NAC) 逆转了这些效应,表明了一个新的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 营养科学 营养科学
- 细胞生物学 细胞生物学
背景情况:
- Th17细胞在炎症性疾病中至关重要,但是异质的.
- 了解Th17细胞亚型对于治疗炎症疾病至关重要.
- 营养素的可用性会影响组织平衡和免疫细胞功能.
研究的目的:
- 研究果糖消费对Th17细胞分化和功能的影响.
- 阐明果糖加剧炎症疾病的机制.
- 为了确定果糖介导病理的潜在治疗点.
主要方法:
- 评估果糖对致病性 (pTh17) 和恒常性Th17细胞分化在体外的影响.
- 使用大肠炎和实验性自身免疫脑膜炎 (EAE) 的小鼠模型.
- 研究活性氧物种 (ROS) 和表皮生长因子受体 (EGFR) 信号传递的作用.
主要成果:
- 果糖可以选择性地增强致病的Th17细胞分化和功能,加剧结肠炎和EAE.
- 果糖增加了pTh17细胞中的代谢活动,ROS产生和EGFR信号传递.
- N-乙半氨酸 (NAC),一种ROS清除剂,改善了高果糖诱导的炎症和疾病严重程度.
结论:
- 高果糖摄入量特别促进致病的Th17细胞反应,恶化炎症性疾病.
- ROS积累和随后的EGFR-STAT3通路激活是关键机制.
- 向ROS或EGFR-STAT3通路可能为pTh17介导疾病提供治疗策略.
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