Component

Indole-3-propionic acid / indolepropionate

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

8 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 it acts on

  1. Indolepropionate alone weakly activated human PXR, with an EC50 near 120 micromolar; adding 1 mM indole enhanced activation.

    Indole-3-propionic acid / indolepropionate → Human pregnane X receptor / SXR / PXR / NR1I2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 1
    experimental_model
    Human PXR reporter in 293T cells.
    limitations
    Millimolar indole is an assay condition, not a verified systemic human exposure.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A partner microbial metabolite changed the human receptor response.
    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

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 530–536

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human PXR reporter in 293T cells. · source_derived_draft · unverified_draft

    ## tryptophan-ipa-human-pxr A partner microbial metabolite changed the human receptor response. Indolepropionate alone weakly activated human PXR, with an EC50 near 120 micromolar; adding 1 mM indole enhanced activation. Model: Human PXR reporter in 293T cells. Limitations: Millimolar indole is an assay condition, not a verified systemic human exposure. Evidence access: Primary full text, Figure 1 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

  2. Indolepropionate activated mouse PXR with an EC50 near 0.55 micromolar in the reporter assay.

    Indole-3-propionic acid / indolepropionate → Mouse pregnane X receptor / Pxr / Nr1i2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, Figure 1
    experimental_model
    Mouse PXR expressed in 293T cells.
    limitations
    Expression host does not make the receptor human; potency differed sharply for human PXR.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The mouse receptor was sensitive to this microbial product.
    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

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 522–528

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse PXR expressed in 293T cells. · source_derived_draft · unverified_draft

    ## tryptophan-ipa-mouse-pxr The mouse receptor was sensitive to this microbial product. Indolepropionate activated mouse PXR with an EC50 near 0.55 micromolar in the reporter assay. Model: Mouse PXR expressed in 293T cells. Limitations: Expression host does not make the receptor human; potency differed sharply for human PXR. Evidence access: Primary full text, Figure 1 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

What acts on it

  1. C. sporogenes acdA disruption impaired the reductive aromatic-amino-acid pathway leading to indolepropionate.

    Clostridium sporogenes AcdA → Indole-3-propionic acid / indolepropionate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 3
    experimental_model
    Bacterial targeted-mutant metabolomics.
    limitations
    Do not equate a host ACAD gene with this microbial enzyme.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A later reduction step is another potential production bottleneck.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 506–512

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Bacterial targeted-mutant metabolomics. · source_derived_draft · unverified_draft

    ## tryptophan-acda-loss A later reduction step is another potential production bottleneck. C. sporogenes acdA disruption impaired the reductive aromatic-amino-acid pathway leading to indolepropionate. Model: Bacterial targeted-mutant metabolomics. Limitations: Do not equate a host ACAD gene with this microbial enzyme. Evidence access: Primary full text, Figure 3 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 evidence

  2. Disrupting fldC in C. sporogenes abolished indolepropionate accumulation in culture and altered aromatic-amino-acid metabolism.

    Clostridium sporogenes FldC → Indole-3-propionic acid / indolepropionate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figures 1–3
    experimental_model
    C. sporogenes ClosTron mutant and LC–MS/MS.
    limitations
    The mutation affects phenylalanine and tyrosine products as well; effects cannot all be assigned to indolepropionate.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A missing microbial enzyme stopped production despite available tryptophan.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 490–496

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C. sporogenes ClosTron mutant and LC–MS/MS. · source_derived_draft · unverified_draft

    ## tryptophan-fldc-loss A missing microbial enzyme stopped production despite available tryptophan. Disrupting fldC in C. sporogenes abolished indolepropionate accumulation in culture and altered aromatic-amino-acid metabolism. Model: C. sporogenes ClosTron mutant and LC–MS/MS. Limitations: The mutation affects phenylalanine and tyrosine products as well; effects cannot all be assigned to indolepropionate. Evidence access: Primary full text, Figures 1–3 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 evidence

  3. C. sporogenes fldH disruption impaired the reductive metabolism of aromatic amino acids needed for indolepropionate production.

    Clostridium sporogenes FldH → Indole-3-propionic acid / indolepropionate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 3
    experimental_model
    Bacterial targeted-mutant metabolomics.
    limitations
    Genetic pathway necessity is not a purified-enzyme substrate-specificity measurement.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The microbial route needs more than one enzyme.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 498–504

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Bacterial targeted-mutant metabolomics. · source_derived_draft · unverified_draft

    ## tryptophan-fldh-loss The microbial route needs more than one enzyme. C. sporogenes fldH disruption impaired the reductive metabolism of aromatic amino acids needed for indolepropionate production. Model: Bacterial targeted-mutant metabolomics. Limitations: Genetic pathway necessity is not a purified-enzyme substrate-specificity measurement. Evidence access: Primary full text, Figure 3 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 evidence

Where it participates (unsigned role)

  1. Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii.

    Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Efficacy of anti-PD-1 checkpoint blockade source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"}
    experimental_model
    Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study
    exposure
    Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people
    limitations
    The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Mouse
    plain_language
    The cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do.
    primary_references
    [bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
    tissue_or_cell_type
    Gut microbiota and tumour microenvironment

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 658–669

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study · source_derived_draft · unverified_draft

    ### bg-a-cereal-glucan-reaches-immunity Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do. organism: Mouse tissue_or_cell_type: Gut microbiota and tumour microenvironment experimental_model: Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study limitations: The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here. exposure: Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people evidence_span: {"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"} [bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
    Complete structured claim and evidence

  2. Gnotobiotic mice colonized with the fldC-mutant strain had reduced gut and circulating indolepropionate and increased intestinal permeability compared with wild-type colonization.

    Clostridium sporogenes FldC → Mouse intestinal permeability in microbial tryptophan experiments source_derived_draftungraded
    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 evidence

  3. Nr1i2-deficient mice had a barrier defect with increased TLR4-related signaling; additional Tlr4 deletion corrected the permeability phenotype.

    Mouse pregnane X receptor / Pxr / Nr1i2 → Mouse intestinal permeability in microbial tryptophan experiments source_derived_draftungraded
    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

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