Component
Mouse intestinal permeability in microbial tryptophan experiments
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
Gnotobiotic mice colonized with the fldC-mutant strain had reduced gut and circulating indolepropionate and increased intestinal permeability compared with wild-type colonization.
Experimental context and source evidence
- evidence_access
- Primary full text, host colonization results
- experimental_model
- Gnotobiotic mouse colonization.
- limitations
- Several metabolites changed; this comparison alone does not prove indolepropionate is the sole mediator.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A microbial genetic change altered a host barrier phenotype.
- primary_references
- A gut bacterial pathway metabolizes aromatic amino acids into nine circulating metabolites. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29168502/ · DOI 10.1038/nature24661
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 514–520
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Gnotobiotic mouse colonization. · source_derived_draft · unverified_draft
## tryptophan-fldc-host-effect A microbial genetic change altered a host barrier phenotype. Gnotobiotic mice colonized with the fldC-mutant strain had reduced gut and circulating indolepropionate and increased intestinal permeability compared with wild-type colonization. Model: Gnotobiotic mouse colonization. Limitations: Several metabolites changed; this comparison alone does not prove indolepropionate is the sole mediator. Evidence access: Primary full text, host colonization results A gut bacterial pathway metabolizes aromatic amino acids into nine circulating metabolites. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29168502/ · DOI 10.1038/nature24661
Complete structured claim and evidenceNr1i2-deficient mice had a barrier defect with increased TLR4-related signaling; additional Tlr4 deletion corrected the permeability phenotype.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text, genetic barrier experiments
- experimental_model
- Mouse Nr1i2 and Tlr4 genetic perturbations.
- limitations
- Does not demonstrate the same causal chain in human patients.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Receptor status and inflammatory sensing determined the barrier outcome.
- primary_references
- Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 538–544
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Nr1i2 and Tlr4 genetic perturbations. · source_derived_draft · unverified_draft
## tryptophan-pxr-tlr4-barrier Receptor status and inflammatory sensing determined the barrier outcome. Nr1i2-deficient mice had a barrier defect with increased TLR4-related signaling; additional Tlr4 deletion corrected the permeability phenotype. Model: Mouse Nr1i2 and Tlr4 genetic perturbations. Limitations: Does not demonstrate the same causal chain in human patients. Evidence access: Primary full text, genetic barrier experiments Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25065623/ · DOI 10.1016/j.immuni.2014.06.014
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.