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. Author manuscript; available in PMC: 2015 Jul 8.
Published in final edited form as: Nature. 2014 Oct 22;517(7533):205–208. doi: 10.1038/nature13828

Figure 4. C. scindens-mediated C. difficile inhibition is associated with secondary bile acid synthesis and dependent on bile endogenous to intestinal content.

Figure 4

Relative abundance of secondary bile species (a) and biosynthesis gene abundance predicted by PICRUSt (b) in intestinal content from antibiotic-exposed C. difficile susceptible (n=21), resistant (n=47), and pre-antibiotic (n=15) animals. Correlation of C. difficile susceptibility with secondary bile acid biosynthesis gene family abundance in intestinal content (n=6) quantified using shotgun sequencing (c). Intestinal abundance of deoxycholic acid (DCA) following adoptive transfer of bacteria (n=10 per group) (d). Correlation of C. scindens engraftment with DCA abundance and baiCD status in intestinal content of antibiotic-exposed, adoptively transferred animals (n=30) (e). Bile acid-dependent C. scindens-mediated inhibition of C. difficile quantified ex vivo (n=6 per group) (f). ****P<0.0001, ***P<0.001, **P<0.01, *P<0.05. Gylceroltransferase F51, endogenous reference gene (c). Shaded region around mean ‘pre-antibiotic (abx)’ DCA abundance (s.d.) (e).