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. Author manuscript; available in PMC: 2018 May 10.
Published in final edited form as: Cell Host Microbe. 2017 May 10;21(5):592–602.e4. doi: 10.1016/j.chom.2017.04.002

Figure 5. Adoptive transfer of bacterial consortia containing C. bolteae and B. producta prevents VRE colonization.

Figure 5

(A–B) Ampicillin-treated mice were orally gavaged with PBS or a mixture of C. bolteae, B. producta, Blautia_unclassified, E. dolichum, A. muciniphila, P. distasonis and B. sartorii (7-mix) for three consecutive days beginning on day 2 of antibiotic treatment. Mice were challenged with VRE the day following the third gavage and fecal samples were collected at the indicated time points. (A) VRE CFUs in stool samples 1, 3 and 6/8 days post inoculation (p.i.) (****P < 0.0001, Mann-Whitney test; n = 10 mice per group). (B) Fecal microbiota composition of treated mice on day 1 p.i. *, 7-mix input. (C) VRE stool burden 3 days p.i. in mice treated with 7-mix consortia lacking individual bacterial strains as described in (A–B). Bu, Blautia_unclassified; Am, A. muciniphila; Ed, E. dolichum; Cb, C. bolteae; Bp, B. producta (n = 3 mice per group). (D) VRE density 3 days p.i. in mice treated with a consortium of four bacterial strains (CBBP) and combinations thereof. Experimental approach described in (A–B) was followed (n = 3–6 mice per group). (E) Relative abundance levels of B. producta and C. bolteae on day 3 p.i. in feces from mice administered the 7-mix, CBBP or bacterial mixtures lacking C. bolteae, B. producta or P. distasonis (Ps) and B. sartorii (Bs) (n = 3–14 mice per group). Δ indicates the absence of corresponding strain (s).