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<p>Inflammatory bowel disease (IBD) arises from complex interactions among genetic susceptibility, immune dysregulation, the intestinal microbiota and environmental factors. Fucosyltransferase 2 (FUT2) regulates mucosal α1,2-fucosylation and the expression of histo-blood group antigens (HBGAs), thereby shaping host-microbe interactions at the intestinal surface. Loss-of-function FUT2 variants define the non-secretor phenotype and have been linked to IBD susceptibility and altered microbial communities. This review summarizes current evidence on FUT2 in IBD, including epithelial glycosylation-microbiota crosstalk, immune and barrier regulation, metabolite-related inflammatory pathways, intestinal stem-cell biology, and enteric nervous system/VIP-related signaling. We also evaluate translational strategies, including functional compensation with the FUT2-dependent human milk oligosaccharide 2′-fucosyllactose (2′-FL), secretor-status-stratified interventions, and preclinical approaches such as L-fucose and D-serine. Overall, FUT2 is an important node connecting host glycosylation, microbial ecology and intestinal immune homeostasis, but its value as a direct therapeutic or biomarker target in IBD remains exploratory. Most mechanistic and causal evidence currently derives from mouse models. Although human genetic and microbiome association data are relatively robust, interventional clinical evidence remains limited, which represents a major barrier to clinical translation.</p>

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FUT2-mediated α1,2-fucosylation in inflammatory bowel disease: mechanisms and translational potential

  • 期刊论文

  • 发表日期：

    2026年7月22日

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  • Jin Chen,
  • Li Gan,
  • Shuhong Zhang,
  • Shengtao Liao,
  • Lin Lv

摘要

Inflammatory bowel disease (IBD) arises from complex interactions among genetic susceptibility, immune dysregulation, the intestinal microbiota and environmental factors. Fucosyltransferase 2 (FUT2) regulates mucosal α1,2-fucosylation and the expression of histo-blood group antigens (HBGAs), thereby shaping host-microbe interactions at the intestinal surface. Loss-of-function FUT2 variants define the non-secretor phenotype and have been linked to IBD susceptibility and altered microbial communities. This review summarizes current evidence on FUT2 in IBD, including epithelial glycosylation-microbiota crosstalk, immune and barrier regulation, metabolite-related inflammatory pathways, intestinal stem-cell biology, and enteric nervous system/VIP-related signaling. We also evaluate translational strategies, including functional compensation with the FUT2-dependent human milk oligosaccharide 2′-fucosyllactose (2′-FL), secretor-status-stratified interventions, and preclinical approaches such as L-fucose and D-serine. Overall, FUT2 is an important node connecting host glycosylation, microbial ecology and intestinal immune homeostasis, but its value as a direct therapeutic or biomarker target in IBD remains exploratory. Most mechanistic and causal evidence currently derives from mouse models. Although human genetic and microbiome association data are relatively robust, interventional clinical evidence remains limited, which represents a major barrier to clinical translation.