Epigenetic regulation by gut microbiota-derived metabolites in celiac disease
A narrative review maps how microbiota metabolites — especially butyrate — modulate epigenetic mechanisms in celiac disease pathogenesis.
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What the study showed
The review describes that dysbiosis in celiac disease involves reduced microbial diversity and depletion of protective taxa such as Bacteroidetes. Butyrate acts protectively by inhibiting histone deacetylases and stabilizing FOXP3 in regulatory T cells. Other microbial metabolites may amplify pro-inflammatory pathways via NF-κB, IL-17, and IFN-γ through epigenetic modifications.
How it was done
This is a narrative literature review consolidating evidence on the microbiota-metabolite-epigenetic axis in celiac disease, incorporating data from organoid models and multi-omics studies.
Risk of bias
Narrative review with no described systematic search, no meta-analysis, and no formal quality assessment of included studies. Organoid and multi-omics data are preliminary and do not establish clinical causality.
What this study does NOT prove
It cannot be concluded that butyrate supplementation or probiotics prevent or treat celiac disease in humans.
In clinical practice
No direct clinical recommendation can be derived from this review. Interventions based on postbiotics or epigenetic modulation remain experimental.
Limitations
Narrative review with no described systematic search, no meta-analysis, and no formal quality assessment of included studies. Organoid and multi-omics data are preliminary and do not establish clinical causality.
Technical appendix
Version history
- 1.0 · 2026-08-11 — Auto-generated under Evidence Standard v1.0
Paid access: structured summary from public metadata; consult the original study at the source.