Butyricimonas virosa AM16-14 attenuates dextran sulfate sodium-induced colitis and shifts mouse fecal metabolomic trajectories

Ulcerative colitis (UC) involves epithelial injury, inflammation, and microbiota-linked metabolism. We evaluated Butyricimonas virosa AM16-14 in an acute dextran sulfate sodium (DSS) colitis mouse experiment, resolved its complete genome, analyzed human UC microbiome data as ecological context, and examined fecal liquid chromatography-mass spectrometry (LC–MS) profiles in positive- and negative-ion modes. AM16-14 carried a 5.00 Mb circular genome with 42.95% GC content and 4,126 predicted coding sequences. Compared with DSS alone, AM16-14-treated mice showed higher final body weight, a lower disease activity index (DAI), longer colons, reduced histological injury, stronger Alcian blue mucin staining, and lower tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6); interleukin-1beta (IL-1beta) and interleukin-10 (IL-10) did not change significantly. The human analysis associated B. virosa with lower focal network connectivity in UC. Positive-ion profiles identified recovery-oriented feature shifts and two dominant recovery trajectories. Complementary negative-ion analysis retained 1,079 features. Complementary genomic screens yielded nine loci associated with antimicrobial resistance (AMR), virulence-associated reference homologies, and one final predicted provirus. A cluster of four AMR-associated loci occurred near transposase annotations. These findings support AM16-14 as a complete-genome-resolved microbiota-directed candidate strain that attenuates multiple acute mouse colitis readouts.