Component

Mouse intestinal antimicrobial peptide expression in tryptophan experiments

Context-specific entity; species, compartment and exposure are stated on each claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Rapamycin reduced mouse intestinal antimicrobial peptides, and nicotinamide did not rescue that reduction.

    Mouse mechanistic target of rapamycin / Mtor → Mouse intestinal antimicrobial peptide expression in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, mTOR results and Supplementary Figure 22 description
    experimental_model
    Mouse mTOR inhibition in vivo.
    limitations
    Rapamycin affects multiple cell types; no human dietary threshold established.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    More precursor or downstream vitamin cannot replace every missing signal.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 98–104

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse mTOR inhibition in vivo. · source_derived_draft · unverified_draft

    ## tryptophan-mtor-block-nam More precursor or downstream vitamin cannot replace every missing signal. Rapamycin reduced mouse intestinal antimicrobial peptides, and nicotinamide did not rescue that reduction. Model: Mouse mTOR inhibition in vivo. Limitations: Rapamycin affects multiple cell types; no human dietary threshold established. Evidence access: Primary full text, mTOR results and Supplementary Figure 22 description ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

  2. A tryptophan-free diet reduced small-intestinal antimicrobial peptide expression and increased chemically induced colitis susceptibility in wild-type mice.

    L-Tryptophan → Mouse intestinal antimicrobial peptide expression in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text, diet experiments
    experimental_model
    Mouse tryptophan-free diet with DSS/TNBS challenges.
    limitations
    Induced susceptibility, not proof that every human colitis case is tryptophan deficiency.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Low dietary supply weakened a gut defense response in mice.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 82–88

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse tryptophan-free diet with DSS/TNBS challenges. · source_derived_draft · unverified_draft

    ## tryptophan-trp-free-peptides Low dietary supply weakened a gut defense response in mice. A tryptophan-free diet reduced small-intestinal antimicrobial peptide expression and increased chemically induced colitis susceptibility in wild-type mice. Model: Mouse tryptophan-free diet with DSS/TNBS challenges. Limitations: Induced susceptibility, not proof that every human colitis case is tryptophan deficiency. Evidence access: Primary full text, diet experiments ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Microbiota transfer from Ace2-mutant mice transmitted increased colitis susceptibility to germ-free wild-type recipients.

    Mouse angiotensin-converting enzyme 2 / Ace2 → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, microbiota-transfer results
    experimental_model
    Mouse donor-to-recipient microbiota transfer.
    limitations
    Transfer does not isolate one bacterial species or one metabolite.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The altered microbial community carried part of the susceptibility.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 106–112

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse donor-to-recipient microbiota transfer. · source_derived_draft · unverified_draft

    ## tryptophan-microbiota-transfer The altered microbial community carried part of the susceptibility. Microbiota transfer from Ace2-mutant mice transmitted increased colitis susceptibility to germ-free wild-type recipients. Model: Mouse donor-to-recipient microbiota transfer. Limitations: Transfer does not isolate one bacterial species or one metabolite. Evidence access: Primary full text, microbiota-transfer results ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards