Fig. 2: Genotoxic K. oxytoca reduce richness of the murine gut microbiota. | Nature Microbiology

Fig. 2: Genotoxic K. oxytoca reduce richness of the murine gut microbiota.

From: Enterotoxin tilimycin from gut-resident Klebsiella promotes mutational evolution and antibiotic resistance in mice

Fig. 2

a, Longitudinal study design. Cohorts received Curam 24 h before gavage with sterile broth (mock); toxigenic K. oxytoca AHC-6, TM/TV deficient ΔnpsB; or ΔnpsB complemented with npsB in trans (pNpsB). Curam was withdrawn 13 days post-infection. Mice were killed on day 20 after 7 days post-antibiotic recovery. b, Quantification of faecal TM and cell counts of K. oxytoca obtained from infected mice (n = 4 per group). Shown is geometric mean of CFU g−1 faeces and mean average concentrations of TM (grey shading) for each group over time (AHC-6, red line; pNpsB, dotted green line). LOQ denotes limit of quantification for TM. Dotted line marks end of Curam treatment. Data for individual mice are presented in Extended Data Fig. 2b. c,e, Comparison of alpha-diversity indices in faeces at day 6 (c) and in caecal content at day 20 (e) post-infection. Box plots (centre lines represent medians, box limits represent upper and lower quartiles, whiskers span minimum to maximum values, all points shown) of observed sequence variants (observed richness, left) and Shannon indices (right) for all treatments. Statistical significance by Kruskal–Wallis (all groups) followed by Kruskal–Wallis (pairwise) analysis. *q < 0.05, after Benjamini–Hochberg FDR correction. d,f, 2D-PCoA plots of Jaccard distance (beta diversity) on day 6 (d) and day 20 (f) post-infection. Statistical significance was evaluated by pairwise PERMANOVA with Benjamini–Hochberg FDR correction (Extended Data Fig. 2), *q < 0.05. Ellipses represent the 95% confidence interval.

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