Mice model Raw sequence reads. mouse gut metagenome

Background: The most widely used and characterized experimental model of ulcerative colitis (UC) is the epithelial erosion, dextran sulfate sodium (DSS)-induced colitis, which is developed by administration of DSS in drinking water. Until recently, much attention has been given to the role of mucosal response to DSS treatment, and only few studies investigated colonic microbiota in relation to DSS. We investigated compositional and functional changes of the microbiomes of the colon tissue and feces in mice treated with DSS. Methods: C57Bl/6 mice received 5% DSS in drinking water for 5 days. Inflammation was evaluated clinically and by analysis of colonic tissue cytokine levels and C-reactive protein (CRP) in the serum. Colonic mucosa and fecal samples were used for DNA extraction and the V4 region of bacterial 16S rRNA was subjected to MiSeq Illumina sequencing. Alpha- and beta-diversities, and differences at the phylum and genus levels were determined, and bacterial functional pathways were predicted. Results: DSS increased disease severity, serum CRP and cytokines IL-1β and IL-6, but decreased bacterial species richness, and shifted bacterial community composition only in the fecal samples. Bacteroides ovatus, Turicibacter, Escherichia, Clostridium, rc4-4, Enterobacteriaceae, Clostridiaceae, Bacteroidaceae, RF39, RF32, and Bacteroidales taxa were associated with DSS treatment. Also, DSS altered microbial functional pathways in both colonic mucosa and fecal samples. Conclusions: The development of colitis in DSS model was accompanied with the disruption of gut microbiota. While colitis development is driven by an interplay between mucosal epithelial damage, an inflammatory response, and a dysbiotic microbiota, it is however, not clear if DSS directly induces dysbiosis, or if microbiota dysbiosis occurs as a result of mucosal damage and inflammatory response.