Inflammatory bowel disease is associated with several genetic risk loci. Loss-of-function mutation in the α1,2-fucosyltransferase (fut2) gene, which alters fucosylation on the surface of intestinal epithelial cells, is one example. However, whether bacterial fucosylation can contribute to gut inflammation is unclear. Here we show that host fucosylation status influences fucosylation biosynthesis by gut commensal bacteria. Mice colonized with faecal microbiota of Fut2 knockout mice or Bacteroides fragilis with lower surface fucosylation are predisposed to colitis. This was supported by human cohort data showing that bacterial fucosylation levels decrease in patients with inflammatory bowel disease and correlate with intestinal inflammation. Using a mouse model for Bacteroides fragilis to explore the role of fucosylation in gut immunity, we show that the fucosylation status of epithelial cells and bacteria is critical for maintaining B cell responses in the gut. Host-derived and dietary fucose mediate immunoglobulin A (IgA) recognition of gut microbiota, and this interaction facilitates the translocation of commensals to Peyer’s patches and alters the immune landscape of Peyer’s patches with increased germinal centre B cells and IgA-secreting antigen-specific B cells. Finally, dietary fucose enhances the IgA response against Salmonella and protects against systemic bacterial dissemination. This highlights the role of host and bacterial fucosylation in maintaining IgA homeostasis and immune escape mechanisms.

炎症性肠病与几个遗传风险位点有关。α1,2-岩藻糖基转移酶 （fut2） 基因的功能丧失突变就是一个例子，它改变了肠上皮细胞表面的岩藻糖基化。然而，细菌岩藻糖基化是否会导致肠道炎症尚不清楚。在这里，我们表明宿主岩藻糖基化状态会影响肠道共生菌的岩藻糖基化生物合成。用 Fut2 敲除小鼠的粪便微生物群或具有较低表面岩藻糖基化的脆弱拟杆菌定植的小鼠易患结肠炎。人类队列数据支持了这一点，该数据显示炎症性肠病患者的细菌岩藻糖基化水平降低，并与肠道炎症相关。使用 Bacteroides fragilis 的小鼠模型来探索岩藻糖基化在肠道免疫中的作用，我们表明上皮细胞和细菌的岩藻糖基化状态对于维持肠道中的 B 细胞反应至关重要。宿主来源和膳食岩藻糖介导免疫球蛋白 A （IgA） 对肠道微生物群的识别，这种相互作用促进共生细胞转移到 Peyer 斑，并随着生发中心 B 细胞和分泌 IgA 的抗原特异性 B 细胞的增加而改变 Peyer 斑的免疫景观。最后，膳食岩藻糖可增强对沙门氏菌的 IgA 反应并防止全身细菌传播。这突出了宿主和细菌岩藻糖基化在维持 IgA 稳态和免疫逃逸机制中的作用。