M. C. Niu, Yan Li, Bo Ma, Meng Xiang-chen
Bifidobacterium bifidum can alleviate intestinal barrier damage, but its reliance on mucin O-glycan modifications remains unclear. A dextran sodium sulfate-induced colitis mouse model was established to evaluate the therapeutic potential of B. bifidum Z29–2, C5, and their mixture. The results demonstrated that B. bifidum alleviated intestinal injury by preventing colon shortening and goblet cell depletion, as well as reducing levels of inflammatory cytokines. Furthermore, B. bifidum maintained the structural integrity of gut microbiota by enriching beneficial bacteria like Faecalibaculum and Olsenella, while suppressing the abundance of opportunistic pathogens, including Mucispirillum and Erysipelatoclostridium . Additionally, strains Z29–2 and C5 promoted goblet cell differentiation and MUC2 secretion by inhibiting of the Notch signaling pathway. Crucially, these strains enhanced mucin fucosylation by upregulating Fut1 and Fut2, while maintaining glycan homeostasis by reducing O-glycan sulfation and chain truncation. This study provides deeper protective mechanism of B. bifidum in colitis and supports its potential application as a functional supplements.