High-fructose corn syrup aggravates colitis via microbiota dysbiosis-mediated Th17/Treg imbalance

被引:10
作者
Zhou, Mingxia [1 ,2 ,3 ]
Liu, Xiaoman [1 ,3 ]
He, Jing [4 ]
Xu, Xinyu [5 ]
Ju, Chenxi [5 ]
Luo, Shangjian [1 ,3 ]
Lu, Xiajuan [6 ]
Du, Peng [7 ]
Chen, Yingwei [1 ,3 ]
机构
[1] Shanghai Jiao Tong Univ, XinHua Hosp, Dept Gastroenterol, Sch Med, Shanghai, Peoples R China
[2] Zhengzhou Univ, Dept Gastroenterol, Affiliated Hosp 1, Zhengzhou, Peoples R China
[3] Shanghai Key Lab Pediat Gastroenterol & Nutr, Shanghai, Peoples R China
[4] Zhengzhou Univ, Dept Breast Surg, Affiliated Hosp 1, Zhengzhou, Peoples R China
[5] Zhengzhou Univ, Dept Med Lab, Affiliated Hosp 1, Zhengzhou, Peoples R China
[6] Kongjiang Hosp Yangpu Dist, Dept Gastroenterol, Shanghai, Peoples R China
[7] Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Colorectal Surg, Sch Med, Shanghai, Peoples R China
基金
中国博士后科学基金;
关键词
INFLAMMATORY-BOWEL-DISEASE; MUCUS BARRIER; GUT; DIET;
D O I
10.1042/CS20230788
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Dietary fructose is widely used in beverages, processed foods, and Western diets as food additives, and is closely related to the increased prevalence of multiple diseases, including inflammatory bowel disease (IBD). However, the detailed mechanism by which high fructose disrupts intestinal homeostasis remains elusive. The present study showed that high-fructose corn syrup (HFCS) administration exacerbated intestinal inflammation and deteriorated barrier integrity. Several in vivo experimental models were utilized to verify the importance of gut microbiota and immune cells in HFCS-mediated dextran sulfate sodium (DSS)-induced colitis. In addition, untargeted metabolomics analysis revealed the imbalance between primary bile acids (PBAs) and secondary bile acids (SBAs) in feces. Hence, high fructose was speculated to modulate gut microbiota community and reduced the relative abundance of Clostridium and Clostridium scindens at genus and species level respectively, followed by a decrease in SBAs, especially isoalloLCA, thereby affecting Th17/Treg cells equilibrium and promoting intestinal inflammation. These findings provide novel insights into the crosstalk between gut flora, bile acids, and mucosal immunity, and highlight potential strategies for precise treatment of IBD.
引用
收藏
页码:1619 / 1635
页数:17
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