A mannose-rich exopolysaccharide-1 isolated from Bifidobacterium breve mitigates ovalbumin-induced intestinal damage in mice by modulation CD4?+?T cell differentiation and inhibiting NF-κB signaling pathway

Ovalbumin (OVA)-induced intestinal injury is a recurrent and potentially fatal condition. Previous studies have highlighted the roles of exopolysaccharides, particularly a mannose-rich (89.59?%) exopolysaccharide-1 (EPS-1) with a molecular weight of 39.9?kDa, isolated from Bifidobacterium breve H4–2, in repairing intestinal barriers and regulating immune responses. In this study, a mouse model of OVA-induced intestinal injury was used to investigate the effects of EPS-1 on intestinal barrier restoration. The results demonstrated that EPS-1 treatment (400?mg/kg. d) significantly reduced the allergic index (3.25?±?0.43) in OVA-challenged mice ( p ?<?0.05), improved the physical integrity of the intestinal barrier by increasing mucin content and goblet cell number in the ileum ( p ?<?0.05). EPS-1 treatment (400?mg/kg. d) also maintained immune barrier integrity by restoring imbalanced CD4?+?T/CD8?+?T ratios from 0.86?±?0.02 to 1.04?±?0.06, regulating Th1/Th2 and Th17/Treg cells balance, as well as inhibited the NF-κB signaling pathway. Furthermore, EPS-1 maintained microbiota homeostasis by increasing the abundances of Ruminococcus , Butyricicoccus , and Muribaculaceae , while reducing Streptococcus and Candidatus arthromitus . This microbiota modulation enhanced the levels of metabolites such as tyrosine, methionine, tryptophan, triglycerides, and salidroside. In conclusion, EPS-1 shows promise as a functional polysaccharide for therapeutic use.

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