The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Gut Microbiota-Produced Succinate Promotes C. difficile Infection after Antibiotic Treatment or Motility Disturbance
Open accessAbstract
Summary 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 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.
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Cites
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BackgroundGlycan foraging in vivo by an intestine-adapted bacterial symbiont
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Self-citationMicrobiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens
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Complex interactions among diet, gastrointestinal transit, and gut microbiota in humanized mice
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Self-citationMeta-analyses of studies of the human microbiota
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Cited by
Introduction to the human gut microbiota
Thursby, E., & Juge, N. (2017) · Biochemical Journal · doi:10.1042/bcj20160510 · Cited by 3,600
Formation of propionate and butyrate by the human colonic microbiota
Louis, P., & Flint, H. J. (2017) · Environmental Microbiology · doi:10.1111/1462-2920.13589 · Cited by 3,028
Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease
Pickard, J. M., Zeng, M. Y., Caruso, R., & Núñez, G. (2017) · Immunological Reviews · doi:10.1111/imr.12567 · Cited by 1,699
Interactions between the microbiota and pathogenic bacteria in the gut
Bäumler, A. J., & Sperandio, V. (2016) · Nature · doi:10.1038/nature18849 · Cited by 1,420
Microbial genes and pathways in inflammatory bowel disease
Schirmer, M., Garner, A., Vlamakis, H., & Xavier, R. J. (2019) · Nature Reviews Microbiology · doi:10.1038/s41579-019-0213-6 · Cited by 956
Metadata
- Authors
- Ferreyra, J. A., Wu, K. J., Hryckowian, A. J., Bouley, D. M., Weimer, B. C., & Sonnenburg, J. L.
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 16
- Issue
- 6
- Pages
- 770-777
- ISSN
- 1931-3128 (ISSN-L)
- OpenAlex
- W2075702858
- Cited by
- 378
- References
- 9
- FWCI
- 12.76
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Gut Microbiota-Produced Succinate Promotes C. difficile Infection after Antibiotic Treatment or Motility Disturbance. https://app.cochat.ai/papers/10.1016/j.chom.2014.11.003
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- Ferreyra, J. A., Wu, K. J., Hryckowian, A. J., Bouley, D. M., Weimer, B. C., & Sonnenburg, J. L. (2014). Gut Microbiota-Produced Succinate Promotes C. difficile Infection after Antibiotic Treatment or Motility Disturbance. Cell Host & Microbe. https://doi.org/10.1016/j.chom.2014.11.003
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