Fig. 2

Two cohorts of C57BL/6 mice bred in two separate facilities differed in the gut microbiota composition and demonstrated different susceptibility to the AOM/DSS colorectal cancer model. (A) A. muciniphila 16S rRNA gene levels in feces of the mice bred in two separate rooms before the AOM/DSS treatment (normalized to 16S rRNA gene). * p < 0.05 by the Wilcoxon test (W = 81, p = 0.037, n = 8−13). Value points shown in red indicate outliers. (B) Experimental design. (C) Tumors in the colon of mice on the day 98 of the experiment. R1 and R2 indicate different mouse colonies. (D) Percentage of mice with detectable tumors in the colon for each group. Differences were tested using the Fisher Exact test (n = 8−13). (E) Number of tumors in mice following AOM/DSS treatment, ** p < 0.01 by the Wilcoxon test (W = 79.5, p = 0.0068, n = 8−13). (F) Colon tissue area (mm²) affected by tumors. ** p < 0.01 by the Wilcoxon test (W = 93, p = 0.0028, n = 8−13). (G) Alpha diversity on the day 98 of the experiment (at the “CRC” time point). No significant differences were identified by the Wilcoxon test (W = 35, p = 0.238, n = 8−13). Value points shown in red indicate outliers. (H) First two axes of principal coordinate analysis (PCoA) of weighted UniFrac distances at the “CRC” time point (n = 8−13). No difference was found with PERMANOVA with 1000 permutations. (I) Relative abundance of the top 15 taxa at the genus level in mice at the “CRC” time point, assessed by 16S rRNA amplicon sequencing (n = 8−13). (J) Body weight loss during three rounds of DSS, expressed as a percentage of the initial body weight (before AOM injection). Differences between groups on each day were tested using pairwise t-test with Benjaminni-Hochberg p-value correction (t = −2.9, df = 18.9, p = 0.017, n = 8−13). * p-value < 0.05.