Bifidobacterium bifidum Alleviate Intestinal Barrier Damage by Regulating the Intestinal Flora and Colonic Mucin O-Glycan Structural Patterns.

B. bifidum treatment prevented colon shortening in DSS-induced colitis mice.

• A dextran sodium sulfate (DSS)-induced colitis mouse model was used to evaluate therapeutic potential of B. bifidum Z29-2, C5, and their mixture.
• DSS treatment caused significant colon shortening, which was alleviated by B. bifidum administration.
• Both individual strains and their mixture were tested for protective effects on intestinal injury.

B. bifidum prevented goblet cell depletion and reduced inflammatory cytokine levels in colitis mice.

• DSS-induced colitis led to goblet cell depletion, which was mitigated by B. bifidum treatment.
• B. bifidum reduced levels of inflammatory cytokines in the colitis mouse model.
• Strains Z29-2 and C5 were both effective in these protective measures.

B. bifidum enriched beneficial bacteria and suppressed opportunistic pathogens in the gut microbiota.

• B. bifidum maintained structural integrity of gut microbiota by enriching beneficial bacteria including Faecalibaculum and Olsenella.
• Treatment suppressed the abundance of opportunistic pathogens including Mucispirillum and Erysipelatoclostridium.
• These microbiota changes were associated with alleviation of intestinal barrier damage.

B. bifidum strains Z29-2 and C5 promoted goblet cell differentiation and MUC2 secretion by inhibiting the Notch signaling pathway.

• Both strains Z29-2 and C5 promoted goblet cell differentiation.
• MUC2 secretion was increased through inhibition of the Notch signaling pathway.
• Notch signaling pathway inhibition was identified as a key mechanistic target of B. bifidum action on goblet cells.

B. bifidum strains enhanced mucin fucosylation by upregulating fucosyltransferase genes Fut1 and Fut2.

• Strains Z29-2 and C5 upregulated expression of Fut1 and Fut2 genes.
• Upregulation of these fucosyltransferases led to enhanced mucin fucosylation.
• Enhanced fucosylation was identified as a crucial component of the protective mechanism against intestinal barrier damage.

B. bifidum maintained glycan homeostasis by reducing O-glycan sulfation and chain truncation.

• Both strains reduced O-glycan sulfation in colonic mucin.
• Chain truncation of O-glycans was also reduced by B. bifidum treatment.
• These changes in O-glycan structural patterns were associated with maintenance of intestinal barrier integrity.
• The study specifically examined colonic mucin O-glycan structural patterns as a mechanism of action.