Modulation of experimental colitis by Enterococcus faecalis, Enterococcus faecium, and Bacillus subtilis: insights...

The roles of Enterococcus faecium (E. faecium), Enterococcus faecalis (E. faecalis), and Bacillus subtilis (B. subtilis) in colitis remain poorly defined, with existing literature presenting inconsistent and often contradictory evidence. This study aimed to elucidate their contributions to inflammatory bowel disease (IBD) using both infectious (non-typhoidal Salmonella enterica serovar Typhimurium, S. typhimurium) and chemical (dextran sulfate sodium, DSS)-induced colitis models. Colitis was induced in C57BL/6 mice via a single oral dose of S. typhimurium (ATCC14028) and/or administration of DSS for seven days. E. faecium (ATCC51559), E. faecalis (ATCC700802), and B. subtilis (MTCC25292) were orally administered. Disease progression was assessed through body weight monitoring, disease activity index (DAI), biochemical assays, and histopathological evaluation of colon tissues. Administration of individual E. faecium strain or E. faecalis strain did not significantly alter disease parameters. However, administered strain of E. faecalis exacerbated colitis severity in the S. typhimurium-induced model. Co-administration of DSS with S. typhimurium resulted in a pronounced aggravation of disease severity, as evidenced by clinical, biochemical, and histological markers. Notably, treatment with B. subtilis showed colitis attenuation, demonstrated by improvements in DAI, colon length, fecal calprotectin levels, and histopathological scores. These disease-modifying effects were associated with decreased colonic expression of pro-inflammatory mediators (CXCL-1, TNF-α, IL-1β) and increased levels of the anti-inflammatory cytokine IL-10. Tested strain of E. faecalis does not induce colitis under steady-state conditions in this model but may aggravate pathogen-induced colitis, whereas E. faecium strain shows no significant effect under the applied experimental conditions. Combined DSS and S. typhimurium exposure induces robust colitis, wherein B. subtilis exhibits potential disease-modifying effect.