Microbial Respiration and Formate Oxidation as Metabolic Signatures of Inflammation-Associated Dysbiosis
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Intestinal inflammation is frequently associated with an alteration of the gut microbiota, termed dysbiosis, which is characterized by a reduced abundance of obligate anaerobic bacteria and an expansion of facultative Proteobacteria such as commensal E. coli. The mechanisms enabling the outgrowth of Proteobacteria during inflammation are incompletely understood. Metagenomic sequencing revealed bacterial formate oxidation and aerobic respiration to be overrepresented metabolic pathways in a chemically induced murine model of colitis. Dysbiosis was accompanied by increased formate levels in the gut lumen. Formate was of microbial origin since no formate was detected in germ-free mice. Complementary studies using commensal E. coli strains as model organisms indicated that formate dehydrogenase and terminal oxidase genes provided a fitness advantage in murine models of colitis. In vivo, formate served as electron donor in conjunction with oxygen as the terminal electron acceptor. This work identifies bacterial formate oxidation and oxygen respiration as metabolic signatures for inflammation-associated dysbiosis.
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Formate is produced by both the microbiota and the host.
“Formate is produced by microbiota and host37,44.”
From Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy (2025) · cites this paper as [44]
Predicted abundance of pyruvate formate lyase increased in EX-FMT recipients, primarily driven by Desulfovibrio, an unclassified Erysipelotrichaceae genus, and in part by Dubosiella.
“predicted abundance of pyruvate formate lyase (pfl)—an essential enzyme for bacterial formate production44—increased in EX-FMT recipients (Figure 5D), primarily driven by Desulfovibrio, an unclassified genus in the Erysipelotrichaceae family and in part by Dubosiella (Erysipelotrichaceae) (Figure S5B).”
From Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy (2025) · cites this paper as [44]
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- Authors
- Hughes, E. R., Winter, M. G., Duerkop, B. A., Spiga, L., Furtado de Carvalho, T., Zhu, W., Gillis, C. C., Büttner, L., Smoot, M. P., Behrendt, C. L., Cherry, S., Santos, R. L., Hooper, L. V., & Winter, S. E.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- University of Pennsylvania (US)
- Universidade Federal de Minas Gerais (BR)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Winter, Sebastian E.
- ORCID
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2017-02
- Volume
- 21
- Issue
- 2
- Pages
- 208-219
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC5313043
- OpenAlex
- W2587154501
- Cited by
- 353
- References
- 56
- Citations by year
- 2026: 29 · 2025: 57 · 2024: 42 · 2023: 35 · 2022: 38 · 2021: 41 · 2020: 46 · 2019: 32 · 2018: 28 · 2017: 5
- FWCI
- 12.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Host & Microbe (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Public Health Service Grants (AI118807, DK102436, AI007520, GM109776)
- The Welch Foundation (I-1858)
- NSF Graduate Research Fellowship (1000194723)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Keywords
- intestinal inflammation, colitis, gut microbiota, formate oxidation, Escherichia coli, Proteobacteria, formate dehydrogenase, terminal oxidase, facultative anaerobes, metabolic signatures, chemically induced colitis, germ-free mice
- MeSH terms
- Gastrointestinal Microbiome, Animals, Colitis, Disease Models, Animal, Escherichia coli, Female, Formates, Inflammation, Intestines, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Proteobacteria, Mice, Dysbiosis
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