Component

Mouse susceptibility to chemically induced colitis in tryptophan experiments

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

5 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.

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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. Gly-Trp feeding restored serum tryptophan and reduced DSS-colitis susceptibility in Ace2-deficient mice, bypassing loss of single-amino-acid uptake.

    Glycyl-L-tryptophan / Gly-Trp dipeptide → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 2 and rescue results
    experimental_model
    Ace2-mutant mouse dietary rescue.
    limitations
    Not a clinical Gly-Trp treatment recommendation or evidence that free tryptophan always bypasses transporter loss.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A dipeptide delivery route bypassed missing transport support.
    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 74–80

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ace2-mutant mouse dietary rescue. · source_derived_draft · unverified_draft

    ## tryptophan-glytrp-bypass A dipeptide delivery route bypassed missing transport support. Gly-Trp feeding restored serum tryptophan and reduced DSS-colitis susceptibility in Ace2-deficient mice, bypassing loss of single-amino-acid uptake. Model: Ace2-mutant mouse dietary rescue. Limitations: Not a clinical Gly-Trp treatment recommendation or evidence that free tryptophan always bypasses transporter loss. Evidence access: Primary full text, Figure 2 and rescue 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

  2. IL-22-dependent mucosal responses supported Candida colonization resistance and protection from inflammation in the mouse microbial-tryptophan study.

    Mouse interleukin-22 / Il22 → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse fungal colonization and mucosal inflammation models.
    limitations
    This protective model does not establish a universally beneficial effect of sustained AHR or IL-22 activation.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The downstream cytokine helped organize mucosal defense.
    primary_references
    Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23973224/ · DOI 10.1016/j.immuni.2013.08.003

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 482–488

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse fungal colonization and mucosal inflammation models. · source_derived_draft · unverified_draft

    ## tryptophan-il22-protection The downstream cytokine helped organize mucosal defense. IL-22-dependent mucosal responses supported Candida colonization resistance and protection from inflammation in the mouse microbial-tryptophan study. Model: Mouse fungal colonization and mucosal inflammation models. Limitations: This protective model does not establish a universally beneficial effect of sustained AHR or IL-22 activation. Evidence access: Primary abstract Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23973224/ · DOI 10.1016/j.immuni.2013.08.003
    Complete structured claim and evidence

  3. 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

  4. Nicotinamide supplementation markedly alleviated colitis and diarrhea in Ace2-deficient mice.

    Nicotinamide → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 2
    experimental_model
    Mouse Ace2 loss and DSS challenge.
    limitations
    Does not establish identical effects for nicotinic acid or human inflammatory bowel disease.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A downstream vitamin B3 form bypassed part of the disturbed pathway.
    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 90–96

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Ace2 loss and DSS challenge. · source_derived_draft · unverified_draft

    ## tryptophan-nam-rescue A downstream vitamin B3 form bypassed part of the disturbed pathway. Nicotinamide supplementation markedly alleviated colitis and diarrhea in Ace2-deficient mice. Model: Mouse Ace2 loss and DSS challenge. Limitations: Does not establish identical effects for nicotinic acid or human inflammatory bowel disease. Evidence access: Primary full text, Figure 2 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. 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

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.

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