| First Author | Guo XK | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 7 | Pages | 112754 |
| PubMed ID | 37405914 | Mgi Jnum | J:338428 |
| Mgi Id | MGI:7511299 | Doi | 10.1016/j.celrep.2023.112754 |
| Citation | Guo XK, et al. (2023) Interactions between host and intestinal crypt-resided biofilms are controlled by epithelial fucosylation. Cell Rep 42(7):112754 |
| abstractText | As highly organized consortia of bacteria, biofilms have long been implicated in aggravating inflammation. However, our understanding regarding in vivo host-biofilm interactions in the complex tissue environments remains limited. Here, we show a unique pattern of crypt occupation by mucus-associated biofilms during the early stage of colitis, which is genetically dependent on bacterial biofilm-forming capacity and restricted by host epithelial alpha1,2-fucosylation. alpha1,2-Fucosylation deficiency leads to markedly augmented crypt occupation by biofilms originated from pathogenic Salmonella Typhimurium or indigenous Escherichia coli, resulting in exacerbated intestinal inflammation. Mechanistically, alpha1,2-fucosylation-mediated restriction of biofilms relies on interactions between bacteria and liberated fucose from biofilm-occupied mucus. Fucose represses biofilm formation and biofilm-related genes in vitro and in vivo. Finally, fucose administration ameliorates experimental colitis, suggesting therapeutic potential of fucose for biofilm-related disorders. This work illustrates host-biofilm interactions during gut inflammation and identifies fucosylation as a physiological strategy for restraining biofilm formation. |
