Component
Cytokine output of butyrate-treated human IBD biopsies
Context-specific entity; species, compartment and exposure are stated on each claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Butyrate reduced TNF and IL-6 secretion by more than 50% in ex-vivo inflamed human IBD biopsies.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human IBD biopsy culture.
- limitations
- Ex-vivo response is not a randomized clinical remission result.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Inflamed patient tissue released less of two cytokines in culture.
- primary_references
- Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 414–420
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human IBD biopsy culture. · source_derived_draft · unverified_draft
## butyrate-ibd-biopsy-cytokines Inflamed patient tissue released less of two cytokines in culture. Butyrate reduced TNF and IL-6 secretion by more than 50% in ex-vivo inflamed human IBD biopsies. Model: Human IBD biopsy culture. Limitations: Ex-vivo response is not a randomized clinical remission result. Evidence access: Primary abstract Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
Complete structured claim and evidenceGPR109A/G-protein inhibition did not remove the tested human monocyte/macrophage anti-inflammatory response to butyrate; HDAC3-related mechanisms were implicated.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human monocytes and THP-1 macrophage experiments.
- limitations
- This does not negate the distinct mouse epithelial IL-18 dependency.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- A receptor important in some models was not required for this tested response.
- primary_references
- Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 430–436
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human monocytes and THP-1 macrophage experiments. · source_derived_draft · unverified_draft
## butyrate-ibd-hcar2-not-required A receptor important in some models was not required for this tested response. GPR109A/G-protein inhibition did not remove the tested human monocyte/macrophage anti-inflammatory response to butyrate; HDAC3-related mechanisms were implicated. Model: Human monocytes and THP-1 macrophage experiments. Limitations: This does not negate the distinct mouse epithelial IL-18 dependency. Evidence access: Primary abstract Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.