Expansion resistance against genotoxic E. coli: protective effects of Bifidobacterium pseudolongum in DSS-induced colitis in mice.

INTRODUCTION

Ulcerative colitis is a chronic inflammatory disease affecting the colon, and its incidence is rising worldwide. Significant alterations to the composition and function of the gut microbiota that favor the expansion of pathobionts have been shown to be involved in ulcerative colitis. One such pathobiont is Escherichia coli strains carrying the pks island (pks+ E. coli) that contribute to mucosal injury and exacerbate inflammation. In this study, we investigated whether microbiota-targeting interventions may restrict pks+ E. coli expansion and mitigate chemically induced colitis in mice.

RESULTS

In mice colonized with the murine pks+ E. coli NC101 strain (EcNC101) in which acute colitis was induced by dextran sulfate sodium, oral administration of putrescine significantly reduced disease severity, histological damage, and inflammatory cytokine expression. 16S rRNA gene sequencing revealed marked shifts in gut microbiota composition following putrescine treatment, characterized by an increase in the relative abundance of Actinobacteriota and a decrease of Proteobacteria phyla. Among these, Bifidobacterium pseudolongum was associated with higher colonic acetate levels and reduced colitis severity. In EcNC101-colonized mice with colitis, B. pseudolongum administration significantly alleviated colitis by increasing acetate levels and activating peroxisome proliferator-activated receptor γ (PPAR-γ). Functional assays suggested that acetate production by B. pseudolongum contributes to competitive inhibition of EcNC101 growth.

CONCLUSIONS

This study highlights the potential of microbiota-modifying interventions, particularly probiotics such as B. pseudolongum, to control pathobionts, reduce inflammation, and improve intestinal health in ulcerative colitis.