The FUT2 loss-of-function mutations are highly prevalent and are associated with inflammatory bowel disease (IBD). To investigate the impact of FUT2 loss-of-function mutation on the gut microbiota in patients with IBD, 81 endoscopically confirmed IBD patients were genotyped and divided into 3 groups: homozygous for functional FUT2 genes (SeSe), with one copy of non-functional FUT2 gene (Sese), or homozygous for non-functional FUT2 genes (sese). Escherichia, which attaches to fucosylated glycoconjugates, was the only abundant genus exhibiting decreased abundance in sese patients. Compared with SeSe or Sese patients, sese patients exhibited higher abundance in CD8⁺ inducing Alistipe and Phascolarctobacterium and Th17 inducing Erysipelotrichaceae UCG-003. Counter-intuitively, butyrate-producing bacteria were more abundant in sese patients. Consistently, metabolomics analysis found higher levels of butyrate in sese patients. Our data support the hypothesis that FUT2 loss-of-function mutation participates in the IBD pathogenesis by decreasing binding sites for adherent bacteria and thus altering the gut microbiota. Decreased abundances of adherent bacteria may allow the overgrowth of bacteria that induce inflammatory T cells, leading to intestinal inflammation. As FUT2 loss-of-function mutations are highly prevalent, the identification of T cell inducing bacteria in sese patients could be valuable for the development of personalized microbial intervention for IBD.

FUT2功能丧失突变非常普遍，并且与炎症性肠病 (IBD) 相关。为了研究FUT2功能丧失突变对 IBD 患者肠道微生物群的影响，对 81 名内镜确诊的 IBD 患者进行了基因分型，并将其分为 3 组：功能性FUT2基因 ( SeSe ) 纯合子，以及一个非功能性 FUT2 基因拷贝。 FUT2基因 ( Sese )，或非功能性FUT2基因 ( sese ) 的纯合子。附着于岩藻糖基化糖缀合物的埃希氏菌是唯一在这些患者中表现出丰度下降的丰富属。与SeSe或Sese患者相比， sese患者在诱导CD8 ⁺的Alistipe和Phascolarctobacter以及诱导Th17的丹毒菌UCG-003中表现出更高的丰度。与直觉相反，这些患者体内产生丁酸盐的细菌更为丰富。代谢组学分析一致发现这些患者的丁酸盐水平较高。我们的数据支持这样的假设： FUT2功能丧失突变通过减少粘附细菌的结合位点从而改变肠道微生物群来参与 IBD 发病机制。粘附细菌丰度的减少可能会导致诱导炎症 T 细胞的细菌过度生长，从而导致肠道炎症。由于FUT2功能丧失突变非常普遍，因此这些患者中 T 细胞诱导细菌的鉴定对于开发针对 IBD 的个性化微生物干预措施可能很有价值。