Gut Microbiota Research Platform

Figure A (Shannon index plot): Statistical comparisons were conducted via one-way ANOVA with Tukey’s multiple comparison post-hoc test, and the overall model P-value = 2 × 10⁻⁷. Groups labeled with distinct lowercase letters show significant intergroup differences at P < 0.05. W0 denotes the original human fecal microbiota inoculum before transplantation; BAW1–BAW5 represent mouse fecal microbiota collected at Weeks 1–5 post-fecal microbiota transplantation (FMT). The Shannon index of the W0 group was significantly higher than all post-transplant groups (P < 0.05), indicating host-selective colonization of intestinal microbes in mice due to interspecies incompatibility, leading to an overall reduction in gut microbial diversity after human FMT.

Figure B (PCoA plot): Principal Coordinate Analysis based on Bray-Curtis distance illustrating gut microbial community structure. PC1 and PC2 explain 44.43% and 22.61% of total microbial variance, respectively. Original W0 microbiota samples were completely separated from all post-transplant groups along the PC1 axis; BAW1 to BAW5 samples exhibited a sequential directional shift along the PC2 axis with prolonged housing time, demonstrating continuous ordered remodeling and gradual stabilization of mouse intestinal microbiota following FMT.

Figure A: Tumor growth curves of MC38 syngeneic tumors in SPF and germ-free (GF) C57BL/6 mice. Without drug intervention, SPF mice exhibited markedly faster tumor proliferation than GF mice, confirming that gut microbiota facilitates in vivo expansion of MC38 tumors.

Figure B: Tumor growth curves of GF tumor-bearing mice treated with gradient doses of anti-mPD1 antibody. G1 = vehicle control; G2/G3/G4 = 1, 3, 10 mg/kg anti-mPD1 administered intraperitoneally twice weekly for 3 consecutive weeks. Tumor growth inhibition (TGI) rose progressively with increasing dosage, demonstrating dose-dependent anti-tumor efficacy of anti-PD1 in GF mice.

Figure C: Tumor growth curves of SPF tumor-bearing mice treated with gradient anti-mPD1 doses. Grouping and administration regimens consistent with Figure B. Tumor growth inhibition rates across all dose groups were substantially higher than corresponding GF groups, revealing that gut microbiota markedly potentiates the anti-tumor activity of anti-PD1 immune checkpoint inhibitors.

Figure A: Body weight dynamics of mice throughout the experimental period. G1 = untreated control; G2 = DSS-induced ulcerative colitis model group; G3 = positive drug intervention group (6TG); G4 = Akkermansia muciniphila intervention group. DSS administration induced significant weight loss in model mice, which was partially alleviated by both 6TG and Akkermansia treatment.

Figure B: Dynamic Disease Activity Index (DAI) scores across groups. DAI scores were significantly elevated in G2 relative to G1; treatment with 6TG and Akkermansia effectively alleviated colitis manifestations and reduced DAI values.

Figure C: Statistical quantification of colon length excised from sacrificed mice. Intergroup comparisons were performed via one-way ANOVA followed by Tukey’s post-hoc multiple comparison test, with statistical significance defined as P < 0.05. DSS exposure triggered colon shortening, while 6TG and Akkermansia supplementation attenuated colon atrophy.

Figure D: Histopathological injury scoring of colon tissues. One-way ANOVA with Tukey’s post-hoc test was used for statistical analysis, and differences with P < 0.05 were considered statistically significant. G2 displayed markedly elevated pathological scores compared with the healthy control group; both 6TG and Akkermansia intervention relieved colon tissue inflammatory damage.