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Cell Host Microbe. 2014 Dec 10;16(6):770-7. doi: 10.1016/j.chom.2014.11.003.

Gut microbiota-produced succinate promotes C. difficile infection after antibiotic treatment or motility disturbance.

Author information

1
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
2
Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
3
Department of Population Health and Reproduction, University of California, Davis, Davis, CA 95616, USA.
4
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: jsonnenburg@stanford.edu.

Abstract

Clostridium difficile is a leading cause of antibiotic-associated diarrhea. The mechanisms underlying C. difficile expansion after microbiota disturbance are just emerging. We assessed the gene expression profile of C. difficile within the intestine of gnotobiotic mice to identify genes regulated in response to either dietary or microbiota compositional changes. In the presence of the gut symbiont Bacteroides thetaiotaomicron, C. difficile induces a pathway that metabolizes the microbiota fermentation end-product succinate to butyrate. The low concentration of succinate present in the microbiota of conventional mice is transiently elevated upon antibiotic treatment or chemically induced intestinal motility disturbance, and C. difficile exploits this succinate spike to expand in the perturbed intestine. A C. difficile mutant compromised in succinate utilization is at a competitive disadvantage during these perturbations. Understanding the metabolic mechanisms involved in microbiota-C. difficile interactions may help to identify approaches for the treatment and prevention of C. difficile-associated diseases.

Comment in

PMID:
25498344
PMCID:
PMC4859344
DOI:
10.1016/j.chom.2014.11.003
[Indexed for MEDLINE]
Free PMC Article

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