Modulation of dextran sodium sulfate-induced colitis in germ-free mice by Enterococcus faecalis-monocolonization

Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are characterized by chronic gastrointestinal inflammation and involve complex interactions of genetic, environmental, and immune factors. Enterococcus faecalis, a gut commensal bacterium, has been implicated in IBD pathogenesis. This study investigated the effects of E. faecalis-monocolonization in germ-free (GF) mice subjected to dextran sulfate sodium (DSS)-induced colitis. We assessed the impact of E. faecalis on colitis severity, inflammation, and intestinal barrier function. In the context of DSS, E. faecalis-colonized mice exhibited reduced anemia and lower fecal calprotectin levels, though fecal albumin levels were elevated. Despite translocation of E. faecalis to mesenteric lymph nodes, no systemic dissemination was observed. Histological analysis showed similar inflammatory patterns in DSS-treated mice, regardless of E. faecalis-colonization, but more severe mucosal damage was noted in the colonized mice. These findings support that E. faecalis plays a dual role in modulating colitis, influencing inflammation, and exacerbating epithelial injury. The study highlights the utility of GF models in understanding microbial contributions to IBD and emphasized how specific bacterial strains may influence disease progression through strain-dependent interactions with the host immune system and intestinal barrier. Further research is needed to elucidate these complex mechanisms.