Component

Interleukin-1 beta / IL1B

Interleukin-1 beta / IL1B; interpretation depends on linked experimental context.

13 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. Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu.

    Particle size of a glucan preparation → Interleukin-1 beta / IL1B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"}
    experimental_model
    Comparison of large and small beta-glucan particles on human dendritic cell cytokine output
    exposure
    Large against small particulate beta-glucans, with assessment of phagocytosis
    limitations
    Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that.
    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
    Human
    plain_language
    Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all.
    primary_references
    [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
    tissue_or_cell_type
    Monocyte-derived dendritic cell

    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 177–188

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of large and small beta-glucan particles on human dendritic cell cytokine output · source_derived_draft · unverified_draft

    ### bg-particle-size-sets-the-cytokines Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu. 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: Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all. organism: Human tissue_or_cell_type: Monocyte-derived dendritic cell experimental_model: Comparison of large and small beta-glucan particles on human dendritic cell cytokine output limitations: Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that. exposure: Large against small particulate beta-glucans, with assessment of phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"} [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
    Complete structured claim and evidence

  2. GABA transporter GAT2 modulates macrophage function and GAT2 deficiency lowers the production of interleukin-1 beta in proinflammatory macrophages, mechanistically GAT2 deficiency boosts the betaine, S-adenosylmethionine and hypoxanthine metabolic pathway to inhibit transcription factor KID3 expression through increased DNA methylation in its promoter region, KID3 regulates oxidative phosphorylation via targeting the expression of related genes and is also critical for NLRP3-ASC-caspase-1 complex formation, and GAT2 deficiency attenuates macrophage-mediated inflammatory responses in vivo including lipopolysaccharide-induced sepsis, infection-induced pneumonia and high-fat diet-induced obesity.

    The GABA transporter GAT2 → Interleukin-1 beta / IL1B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/33827820.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff", "start_char": 0, "end_char": 1140, "text_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff"}
    experimental_model
    Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models
    exposure
    GAT2 deficiency in macrophages, with lipopolysaccharide sepsis, infection-induced pneumonia and high-fat diet models
    limitations
    The mechanism assigned here is metabolic and transcriptional, running through methylation of a transcription factor promoter, rather than an electrophysiological one.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Mouse
    plain_language
    Taking away the carrier that moves GABA into the macrophage lowered its main inflammatory output, through a metabolic route and not an electrical one.
    primary_references
    [gb-p33827820] GABA transporter sustains IL-1β production in macrophages. (2021). https://pubmed.ncbi.nlm.nih.gov/33827820/ DOI: 10.1126/sciadv.abe9274
    tissue_or_cell_type
    Proinflammatory macrophage

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 560–571

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models · source_derived_draft · unverified_draft

    ### gb-the-transporter-sustains-il1b GABA transporter GAT2 modulates macrophage function and GAT2 deficiency lowers the production of interleukin-1 beta in proinflammatory macrophages, mechanistically GAT2 deficiency boosts the betaine, S-adenosylmethionine and hypoxanthine metabolic pathway to inhibit transcription factor KID3 expression through increased DNA methylation in its promoter region, KID3 regulates oxidative phosphorylation via targeting the expression of related genes and is also critical for NLRP3-ASC-caspase-1 complex formation, and GAT2 deficiency attenuates macrophage-mediated inflammatory responses in vivo including lipopolysaccharide-induced sepsis, infection-induced pneumonia and high-fat diet-induced obesity. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: Taking away the carrier that moves GABA into the macrophage lowered its main inflammatory output, through a metabolic route and not an electrical one. organism: Mouse tissue_or_cell_type: Proinflammatory macrophage experimental_model: Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models limitations: The mechanism assigned here is metabolic and transcriptional, running through methylation of a transcription factor promoter, rather than an electrophysiological one. exposure: GAT2 deficiency in macrophages, with lipopolysaccharide sepsis, infection-induced pneumonia and high-fat diet models evidence_span: {"source_cache": "artifacts/gaba-research/33827820.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff", "start_char": 0, "end_char": 1140, "text_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff"} [gb-p33827820] GABA transporter sustains IL-1β production in macrophages. (2021). https://pubmed.ncbi.nlm.nih.gov/33827820/ DOI: 10.1126/sciadv.abe9274
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice.

    Beta-glucan → Expansion of myeloid-lineage progenitors in the bone marrow source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"}
    experimental_model
    Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models
    exposure
    Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy
    limitations
    A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow.
    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 change is not only in the cells circulating now; it reaches the factory that makes the next ones.
    primary_references
    [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    tissue_or_cell_type
    Bone marrow

    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 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models · source_derived_draft · unverified_draft

    ### bg-training-reaches-the-marrow Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice. 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 change is not only in the cells circulating now; it reaches the factory that makes the next ones. organism: Mouse tissue_or_cell_type: Bone marrow experimental_model: Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models limitations: A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow. exposure: Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy evidence_span: {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"} [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    Complete structured claim and evidence

  2. K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss.

    Intracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes.
    limitations
    Artificial cellular depletion; not a blood threshold or dietary inflammation experiment.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Experimentally losing cellular potassium could trigger this immune sensor.
    primary_references
    [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    tissue_or_cell_type
    Bone-marrow macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 857–866

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. · source_derived_draft · unverified_draft

    ### k-macrophage-loss-nlrp3 K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Experimentally losing cellular potassium could trigger this immune sensor. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. limitations: Artificial cellular depletion; not a blood threshold or dietary inflammation experiment. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    Complete structured claim and evidence

  3. In unstimulated THP-1 cells, stevioside induced TNF, IL-1beta and nitric oxide release; anti-TLR4 antibody partially neutralized TNF release.

    Stevioside → Human unstimulated THP-1 cytokine release source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human THP-1 cells; antibody perturbation.
    limitations
    This is an explained stimulus difference, not a contradiction or proof of a clinical immune benefit.
    nutrient_topic
    Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia
    plain_language
    The same compound can stimulate resting cells while suppressing an already stimulated response.
    primary_references
    Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

    Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 330–336

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human THP-1 cells; antibody perturbation. · source_derived_draft · unverified_draft

    ## stevia-immune-resting The same compound can stimulate resting cells while suppressing an already stimulated response. In unstimulated THP-1 cells, stevioside induced TNF, IL-1beta and nitric oxide release; anti-TLR4 antibody partially neutralized TNF release. Model: Human THP-1 cells; antibody perturbation. Limitations: This is an explained stimulus difference, not a contradiction or proof of a clinical immune benefit. Evidence access: Primary abstract Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465
    Complete structured claim and evidence

  4. Stevioside at 1 mM suppressed LPS-induced TNF and IL-1beta release in human THP-1 cells, with suppression of IKKbeta and NF-kappaB activation.

    Stevioside → Human THP-1 LPS-induced cytokine release source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human monocyte-derived cell line with LPS stimulation.
    limitations
    High direct exposure is not demonstrated after dietary sweetener use; pathway inhibition does not establish direct protein binding.
    nutrient_topic
    Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia
    plain_language
    The inflammatory state changes what the compound does.
    primary_references
    Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

    Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 322–328

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human monocyte-derived cell line with LPS stimulation. · source_derived_draft · unverified_draft

    ## stevia-immune-stimulated The inflammatory state changes what the compound does. Stevioside at 1 mM suppressed LPS-induced TNF and IL-1beta release in human THP-1 cells, with suppression of IKKbeta and NF-kappaB activation. Model: Human monocyte-derived cell line with LPS stimulation. Limitations: High direct exposure is not demonstrated after dietary sweetener use; pathway inhibition does not establish direct protein binding. Evidence access: Primary abstract Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465
    Complete structured claim and evidence

  5. Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta.

    Indicaxanthin → Epithelial permeability of human Caco-2 monolayers source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 317–325

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-barrier Indicaxanthin prevented the increase in epithelial permeability caused by IL-1beta. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  6. Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells.

    Indicaxanthin → Cyclooxygenase-2 (PTGS2) source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 277–285

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-cox2 Indicaxanthin reduced induced COX-2 expression in IL-1beta-exposed Caco-2 cells. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  7. Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.

    Indicaxanthin → NF-kappaB activation in human Caco-2 cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 267–275

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-nfkb Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  8. Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells.

    Indicaxanthin → Human inducible nitric oxide synthase / iNOS / NOS2 source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 287–295

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-nos2 Indicaxanthin reduced induced nitric oxide synthase expression in IL-1beta-exposed Caco-2 cells. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  9. Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.

    Indicaxanthin → Human NADPH oxidase 1 / NOX1 source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 257–265

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-nox1 Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  10. Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.

    Indicaxanthin → Reactive oxygen species generation in human Caco-2 cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 297–305

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-ros Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    Complete structured claim and evidence

  11. Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols.

    Indicaxanthin → Total thiol content in human Caco-2 cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
    duration
    24 h for mediator release and permeability; earlier signaling assays
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Differentiated human Caco-2 intestinal epithelial monolayers
    limitations
    No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Differentiated human Caco-2 intestinal epithelial monolayers
    plain_language
    Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols.
    primary_references
    Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    route
    In vitro co-incubation
    tissue
    Intestinal epithelial model

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 307–315

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft

    ## betalains-caco2-thiols Indicaxanthin prevented IL-1beta-associated loss of total cellular thiols. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
    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