Hydrogen gas and the gut microbiota are potential biomarkers for the development of experimental colitis in mice
Fujiki Y, Tanaka T, Yakabe K, Seki N, Akiyama M, Uchida K, Kim YG. · Gut Microbiome. 2023;5:e3.
Study at a glance
Preclinical
Six-week-old male C57BL/6J mice given dextran sulfate sodium (DSS) or non-sulfated dextran control.
No H₂ treatment was administered. Endogenously produced cage H₂ from breath, skin, flatus and feces was continuously sampled during colitis/control exposure. · H₂ was measured by sensor gas chromatography with a 1,000-ppb detection limit at an average sampling rate of about ten points/hour.
Fifteen days, with DSS/dextran on days 0–5 and repeated gas, weight, fecal LCN2 and microbiome measurements.
Cage H₂ fell as DSS inflammation worsened and was negatively correlated with LCN2 and positively with body weight; H₂ AUC for the chosen LCN2 threshold was 0.75, lower than H₂S at 0.833. Several bacterial families correlated with H₂/inflammation. This was association only and did not test whether H₂ caused, prevented or treated colitis.
Small cage-level mouse experiment, repeated observations not independent animals, mixed breath/skin/fecal gas, observational correlations, selected biomarker threshold and no external validation. Japanese public grants funded the work; authors reported no conflicts.
What kind of evidence is this?
Preclinical
Longitudinal mouse cage-biogas and microbiome observational experiment during DSS colitis
Gastrointestinal health
Other forms
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
Six-week-old male C57BL/6J mice given dextran sulfate sodium (DSS) or non-sulfated dextran control.
Five mice per cage/group, monitored for 15 days; experiments were reported as independently repeated three times.
Fifteen days, with DSS/dextran on days 0–5 and repeated gas, weight, fecal LCN2 and microbiome measurements.
No H₂ treatment was administered. Endogenously produced cage H₂ from breath, skin, flatus and feces was continuously sampled during colitis/control exposure.
Biologically generated endogenous H₂ — neither H₂-only therapy nor Brown's gas.
H₂ was measured by sensor gas chromatography with a 1,000-ppb detection limit at an average sampling rate of about ten points/hour.
2% DSS for five days versus 2% dextran control, followed by tap water and longitudinal within-group measurements.
Outcomes and reported result
Five cage biogases, body weight, fecal lipocalin-2, 16S microbiome composition, correlations and ROC AUC for experimental colitis.
Cage H₂ fell as DSS inflammation worsened and was negatively correlated with LCN2 and positively with body weight; H₂ AUC for the chosen LCN2 threshold was 0.75, lower than H₂S at 0.833. Several bacterial families correlated with H₂/inflammation. This was association only and did not test whether H₂ caused, prevented or treated colitis.
The complete free PMC article, methods, figures and disclosures were checked for endogenous-versus-administered H₂, cage-level sampling, controls, sample/repeats, correlations/ROC, limitations, funding and conflicts.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Small cage-level mouse experiment, repeated observations not independent animals, mixed breath/skin/fecal gas, observational correlations, selected biomarker threshold and no external validation. Japanese public grants funded the work; authors reported no conflicts.
Potential non-invasive biomarker in DSS mouse colitis; it does not validate a human IBD test or an H₂ treatment.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 39290658 · DOI: 10.1017/gmb.2023.17
Free full article in PubMed Central.
Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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