Component

NLRP3 inflammasome

NLRP3 inflammasome; interpretation depends on linked experimental context.

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 acts on it

  1. Nattokinase inhibited NLRP3 inflammasome formation in endothelial cells.

    Nattokinase / subtilisin NAT → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Endothelial cells
    exposure
    Nattokinase
    limitations
    Placed downstream of autophagy induction by the necessity experiments rather than measured as an independent arm.
    organism
    Endothelial cells
    plain_language
    Nattokinase inhibited NLRP3 inflammasome formation in endothelial cells.
    primary_references
    Nattokinase attenuates endothelial inflammation through the activation of SRF and THBS1. (2024) https://pubmed.ncbi.nlm.nih.gov/38679250/ DOI: 10.1016/j.ijbiomac.2024.131779
    route
    In vitro
    tissue
    Cultured endothelium

    Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 631–631

    Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Endothelial cells · source_derived_draft · unverified_draft

    Nattokinase inhibited NLRP3 inflammasome formation in endothelial cells.
    Complete structured claim and evidence

  2. NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction.

    NIMA-related kinase 7 / NEK7 → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays.
    limitations
    NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Potassium loss signals through an assembly protein before caspase activation.
    primary_references
    [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    tissue_or_cell_type
    Bone-marrow macrophages

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 880–889

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. · source_derived_draft · unverified_draft

    ### k-efflux-nek7-assembly NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium loss signals through an assembly protein before caspase activation. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. limitations: NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7. [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    Complete structured claim and evidence

  3. Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles.

    Extracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Primed mouse macrophages, extracellular-K titration.
    exposure
    Artificial extracellular potassium elevation; not dietary excess.
    limitations
    Stimulus-specific; does not justify elevating blood potassium.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Reducing the outward potassium gradient blocked these activation routes.
    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

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 868–878

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primed mouse macrophages, extracellular-K titration. · source_derived_draft · unverified_draft

    ### k-high-medium-nlrp3-block Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing the outward potassium gradient blocked these activation routes. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Primed mouse macrophages, extracellular-K titration. limitations: Stimulus-specific; does not justify elevating blood potassium. exposure: Artificial extracellular potassium elevation; not dietary excess. [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

  4. Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments.

    Imiquimod → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis.
    limitations
    Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse experimental systems
    plain_language
    Some drug-triggered inflammasome routes bypass potassium loss.
    primary_references
    [gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
    tissue_or_cell_type
    Myeloid cells

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 891–900

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. · source_derived_draft · unverified_draft

    ### k-independent-drug-nlrp3 Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some drug-triggered inflammasome routes bypass potassium loss. organism: Mouse experimental systems tissue_or_cell_type: Myeloid cells experimental_model: Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. limitations: Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments. [gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
    Complete structured claim and evidence

  5. 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

Where it participates (unsigned role)

  1. Adding 1 mM ergothioneine for 24 hours reduced IL-18 production in placental explants from women with gestational diabetes.

    L-Ergothioneine → Human interleukin 18 / IL18 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human placental explants; comparison with NLRP3 inhibitor MCC950.
    limitations
    Ex vivo result, not a pregnancy intervention trial or proof of direct NLRP3 binding.
    nutrient_topic
    Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
    plain_language
    Inflammatory output fell in tissue studied outside the body.
    primary_references
    L-ergothioneine reduces mitochondrial-driven NLRP3 activation in gestational diabetes mellitus. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38029485/ · DOI 10.1016/j.jri.2023.104171

    Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 376–382

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human placental explants; comparison with NLRP3 inhibitor MCC950. · source_derived_draft · unverified_draft

    ## ergothioneine-placenta-il18 Inflammatory output fell in tissue studied outside the body. Adding 1 mM ergothioneine for 24 hours reduced IL-18 production in placental explants from women with gestational diabetes. Model: Human placental explants; comparison with NLRP3 inhibitor MCC950. Limitations: Ex vivo result, not a pregnancy intervention trial or proof of direct NLRP3 binding. Evidence access: Primary abstract L-ergothioneine reduces mitochondrial-driven NLRP3 activation in gestational diabetes mellitus. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38029485/ · DOI 10.1016/j.jri.2023.104171
    Complete structured claim and evidence

  2. BHB reduced ASC oligomerization and speck formation.

    D-(R)-beta-hydroxybutyrate → ASC oligomerization and speck formation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    NLRP3 activation models.
    limitations
    Effect did not require HCAR2, AMPK, autophagy or ketone oxidation.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    The inflammatory complex assembled less effectively.
    primary_references
    The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 376–382

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · NLRP3 activation models. · source_derived_draft · unverified_draft

    ## fast-bhb-asc The inflammatory complex assembled less effectively. BHB reduced ASC oligomerization and speck formation. Model: NLRP3 activation models. Limitations: Effect did not require HCAR2, AMPK, autophagy or ketone oxidation. Evidence access: Primary abstract The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804
    Complete structured claim and evidence

  3. BHB reduced NLRP3-mediated IL-1beta and IL-18 production in human monocytes.

    D-(R)-beta-hydroxybutyrate → Human monocyte IL-1beta and IL-18 production source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human monocyte experiments.
    limitations
    Not universal anti-inflammatory activity or a clinical fasting outcome.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    The cellular signal changed selected cytokine outputs.
    primary_references
    The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 384–390

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human monocyte experiments. · source_derived_draft · unverified_draft

    ## fast-bhb-cytokines The cellular signal changed selected cytokine outputs. BHB reduced NLRP3-mediated IL-1beta and IL-18 production in human monocytes. Model: Human monocyte experiments. Limitations: Not universal anti-inflammatory activity or a clinical fasting outcome. Evidence access: Primary abstract The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804
    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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