高果糖玉米糖通过微生物群失调调的Th17/Treg不平衡加剧结肠炎
Mingxia Zhou1,2,3, Xiaoman Liu1,3, Jing He4
1Department of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Clinical science (London, England : 1979)
|October 11, 2023
概括
高果糖摄入量通过破坏肠道微生物群和胆酸代谢而加剧肠道炎症,影响免疫细胞平衡. 这导致肠道屏障受损,恶化诸如炎症性肠病 (IBD) 等疾病.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 饮食中的果糖在西方饮食中很常见,与增加疾病患病率有关,包括炎症性肠病 (IBD).
- 高果糖消费破坏肠道平衡的确切机制尚未完全理解.
研究的目的:
- 为了研究高果糖玉米糖 (HFCS) 如何影响肠道炎症和屏障完整性.
- 阐明肠道微生物群和免疫细胞在HFCS诱导的大肠炎中的作用.
- 探索HFCS对胆酸代谢的影响及其与肠道健康的联系.
主要方法:
- 使用了硫酸 (DSS) 诱导的大肠炎的体内实验模型.
- 对便样本进行非向的代谢学分析.
- 评估了肠道微生物群组成的变化,重点是Clostridium物种.
- 评估了Th17/Treg免疫细胞的平衡.
主要成果:
- 在大肠炎模型中,HFCS的使用加剧了肠道炎症和屏障功能障碍.
- 代谢学揭示了初级胆酸 (PBA) 和二次胆酸 (SBA) 之间的不平衡.
- HFCS减少了Clostridium和Clostridium scindens的丰富性,导致SBAs的减少,特别是isoalloLCA.
- 这些变化影响了Th17/Treg细胞平衡,促进了炎症.
结论:
- 高果糖消费调节肠道微生物群,减少有益的SBA,破坏免疫细胞平衡,导致肠道炎症.
- 研究结果显示,在果糖摄入的背景下,肠道菌群,胆汁酸和粘膜免疫之间存在一种新的交叉声.
- 这些见解表明IBD针对肠道微生物群和胆酸代谢的潜在治疗策略.
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