Component

Crystalline silica / quartz particles

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

14 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. Phagocytosed silica caused lysosomal swelling and leakage in mouse macrophages.

    Crystalline silica / quartz particles → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophage imaging of vesicular cargo redistribution.
    limitations
    Particle preparation and cellular priming matter. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Particles can damage the compartment that engulfs them.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 424–430

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage imaging of vesicular cargo redistribution. · source_derived_draft · unverified_draft

    ## silica-lysosome-damage Particles can damage the compartment that engulfs them. Phagocytosed silica caused lysosomal swelling and leakage in mouse macrophages. Model: Mouse macrophage imaging of vesicular cargo redistribution. Limitations: Particle preparation and cellular priming matter. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step.

    CA-074-Me treatment of silica-exposed mouse macrophages → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophages; 10 micromolar CA-074-Me.
    limitations
    Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A lysosomal protease inhibitor reduced inflammatory output.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 448–454

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; 10 micromolar CA-074-Me. · source_derived_draft · unverified_draft

    ## silica-cathepsin-inhibitor A lysosomal protease inhibitor reduced inflammatory output. CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step. Model: Mouse macrophages; 10 micromolar CA-074-Me. Limitations: Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

  2. Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study.

    Mouse cathepsin B → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse bone-marrow macrophages with silica/MSU comparisons.
    limitations
    Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Genetic loss did not reproduce the inhibitor-based necessity claim.
    primary_references
    Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 472–478

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse bone-marrow macrophages with silica/MSU comparisons. · source_derived_draft · unverified_draft

    ## silica-cathepsin-knockout Genetic loss did not reproduce the inhibitor-based necessity claim. Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study. Model: Mouse bone-marrow macrophages with silica/MSU comparisons. Limitations: Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
    Complete structured claim and evidence

  3. U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages.

    Cholesterol → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Pharmacologically altered lysosomal cholesterol handling.
    limitations
    Not evidence that raising blood cholesterol or dietary cholesterol protects the lung.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Membrane-lipid handling can modify the response to particles.
    primary_references
    Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 496–502

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacologically altered lysosomal cholesterol handling. · source_derived_draft · unverified_draft

    ## silica-cholesterol-lysosome Membrane-lipid handling can modify the response to particles. U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages. Model: Pharmacologically altered lysosomal cholesterol handling. Limitations: Not evidence that raising blood cholesterol or dietary cholesterol protects the lung. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
    Complete structured claim and evidence

  4. Human MARCO expression in CHO cells supported silica binding and apoptosis.

    Human MARCO → Response of human-MARCO-transfected hamster cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human construct in Chinese hamster ovary cells.
    limitations
    Not direct observation of human lung exposure or a universal uptake route.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A human receptor was tested in a nonhuman host cell.
    primary_references
    MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 416–422

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human construct in Chinese hamster ovary cells. · source_derived_draft · unverified_draft

    ## silica-human-marco-binding A human receptor was tested in a nonhuman host cell. Human MARCO expression in CHO cells supported silica binding and apoptosis. Model: Human construct in Chinese hamster ovary cells. Limitations: Not direct observation of human lung exposure or a universal uptake route. Evidence access: Primary abstract MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
    Complete structured claim and evidence

  5. MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake.

    Mouse MARCO → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Primary mouse macrophages; silica 100 micrograms/mL.
    limitations
    Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Less uptake did not necessarily mean less inflammation.
    primary_references
    Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 488–494

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse macrophages; silica 100 micrograms/mL. · source_derived_draft · unverified_draft

    ## silica-marco-lysosome-loss Less uptake did not necessarily mean less inflammation. MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake. Model: Primary mouse macrophages; silica 100 micrograms/mL. Limitations: Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
    Complete structured claim and evidence

  6. MARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages.

    Mouse MARCO → Silica uptake in mouse alveolar macrophages source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Primary mouse macrophages; receptor-null and antibody experiments.
    limitations
    Mouse strain matters: BALB/c uptake was not blocked by the same receptor antibodies.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A scavenger receptor can gate particle entry.
    primary_references
    MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 408–414

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse macrophages; receptor-null and antibody experiments. · source_derived_draft · unverified_draft

    ## silica-marco-uptake A scavenger receptor can gate particle entry. MARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages. Model: Primary mouse macrophages; receptor-null and antibody experiments. Limitations: Mouse strain matters: BALB/c uptake was not blocked by the same receptor antibodies. Evidence access: Primary abstract MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16984918/ · DOI 10.1074/jbc.M605229200
    Complete structured claim and evidence

  7. Nlrp3-deficient macrophages failed to mount the normal silica-induced caspase-1/IL-1 beta response.

    Mouse NLRP3 → Caspase-1 activation after silica in mouse macrophages source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    LPS-primed mouse macrophage genetic comparison.
    limitations
    Priming and activation are separate; dietary silicon is not the particle stimulus. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    The sensor is a distinct necessary component in this model.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 440–446

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · LPS-primed mouse macrophage genetic comparison. · source_derived_draft · unverified_draft

    ## silica-nlrp3-loss The sensor is a distinct necessary component in this model. Nlrp3-deficient macrophages failed to mount the normal silica-induced caspase-1/IL-1 beta response. Model: LPS-primed mouse macrophage genetic comparison. Limitations: Priming and activation are separate; dietary silicon is not the particle stimulus. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

  8. Cybb/gp91phox-deficient macrophages retained silica-triggered inflammasome responses.

    Mouse CYBB / gp91phox → Mouse silica inflammasome response source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophage genetic comparison.
    limitations
    Does not exclude every ROS source or establish NADPH depletion. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    The phagocyte NADPH oxidase burst was not obligatory in this model.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 456–462

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage genetic comparison. · source_derived_draft · unverified_draft

    ## silica-nox2-null The phagocyte NADPH oxidase burst was not obligatory in this model. Cybb/gp91phox-deficient macrophages retained silica-triggered inflammasome responses. Model: Mouse macrophage genetic comparison. Limitations: Does not exclude every ROS source or establish NADPH depletion. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

  9. NFS-rich silica strongly adsorbed zwitterionic phospholipid assemblies and disrupted their order more than negatively charged liposomes.

    Nearly free surface silanols on silica particles → Phosphatidylcholine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Model membranes and computational recognition analysis.
    limitations
    Membrane interaction is not evidence that choline intake increases silica injury or protects against it.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    The phosphocholine headgroup creates a molecular link to membrane composition.
    primary_references
    Molecular recognition between membrane epitopes and nearly free surface silanols explains silica membranolytic activity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35738078/ · DOI 10.1016/j.colsurfb.2022.112625

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 400–406

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Model membranes and computational recognition analysis. · source_derived_draft · unverified_draft

    ## silica-phosphocholine-recognition The phosphocholine headgroup creates a molecular link to membrane composition. NFS-rich silica strongly adsorbed zwitterionic phospholipid assemblies and disrupted their order more than negatively charged liposomes. Model: Model membranes and computational recognition analysis. Limitations: Membrane interaction is not evidence that choline intake increases silica injury or protects against it. Evidence access: Primary full text Molecular recognition between membrane epitopes and nearly free surface silanols explains silica membranolytic activity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35738078/ · DOI 10.1016/j.colsurfb.2022.112625
    Complete structured claim and evidence

  10. High extracellular potassium blocked silica-induced caspase-1 processing and IL-1 beta release, including during low-dose uptake blockade.

    Potassium ion → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophages; 130 mM KCl experimental condition.
    limitations
    Not a potassium supplement treatment; no specific channel identity was established.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    The potassium gradient gates this inflammatory response.
    primary_references
    Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 480–486

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; 130 mM KCl experimental condition. · source_derived_draft · unverified_draft

    ## silica-potassium-gate The potassium gradient gates this inflammatory response. High extracellular potassium blocked silica-induced caspase-1 processing and IL-1 beta release, including during low-dose uptake blockade. Model: Mouse macrophages; 130 mM KCl experimental condition. Limitations: Not a potassium supplement treatment; no specific channel identity was established. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
    Complete structured claim and evidence

  11. Particle surface treatments linked nearly free silanols to membranolysis and inflammatory activity.

    Nearly free surface silanols on silica particles → Membrane disruption by silica particles source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program.
    limitations
    Surface motif is not a dissolved nutrient species; no oral-dose inference.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Surface chemistry helps explain why silica preparations differ.
    primary_references
    Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33097669/ · DOI 10.1073/pnas.2008006117

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 392–398

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program. · source_derived_draft · unverified_draft

    ## silica-silanol-membrane Surface chemistry helps explain why silica preparations differ. Particle surface treatments linked nearly free silanols to membranolysis and inflammatory activity. Model: Characterized quartz/amorphous particles, membrane assays, macrophages and rat exposure program. Limitations: Surface motif is not a dissolved nutrient species; no oral-dose inference. Evidence access: Primary full text Nearly free surface silanols are the critical molecular moieties that initiate the toxicity of silica particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33097669/ · DOI 10.1073/pnas.2008006117
    Complete structured claim and evidence

  12. Cytochalasin D blocked silica uptake and IL-1 beta release, supporting a phagocytosis-dependent interpretation.

    Cytochalasin-D uptake blockade in the 2008 silica study → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophages; related human PBMC result separately reported in the paper.
    limitations
    Inhibitor dose and non-uptake effects require comparison with later low-dose experiments. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Blocking engulfment also blocked inflammatory output in this experiment.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 432–438

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; related human PBMC result separately reported in the paper. · source_derived_draft · unverified_draft

    ## silica-uptake-block-2008 Blocking engulfment also blocked inflammatory output in this experiment. Cytochalasin D blocked silica uptake and IL-1 beta release, supporting a phagocytosis-dependent interpretation. Model: Mouse macrophages; related human PBMC result separately reported in the paper. Limitations: Inhibitor dose and non-uptake effects require comparison with later low-dose experiments. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

  13. Low-dose cytochalasin D blocked silica engulfment while preserving caspase-1 processing and IL-1 beta release.

    Low-dose cytochalasin D in the 2014 silica study → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D.
    limitations
    Immobilized epoxy-crystal experiments used MSU, not silica; do not transfer that detail between materials.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Surface-associated crystals could still trigger a response when uptake was blocked.
    primary_references
    Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 464–470

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D. · source_derived_draft · unverified_draft

    ## silica-uptake-block-2014 Surface-associated crystals could still trigger a response when uptake was blocked. Low-dose cytochalasin D blocked silica engulfment while preserving caspase-1 processing and IL-1 beta release. Model: Mouse bone-marrow macrophages; 0.25–0.5 micromolar cytochalasin D. Limitations: Immobilized epoxy-crystal experiments used MSU, not silica; do not transfer that detail between materials. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
    Complete structured claim and evidence

In the sources

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

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