Component

Mouse caspase-1

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

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

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

Where it participates (unsigned role)

  1. 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

  2. Silica nanoparticles increased inflammasome/pyroptosis-associated markers; MCC950 suppressed the response.

    Silica nanoparticles, 2022 RAW-ASC preparation → Pyroptosis-associated response in mouse RAW-ASC cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles.
    limitations
    Do not assume all sizes, coatings or amorphous preparations behave identically.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A nanoparticle preparation was examined separately from quartz.
    primary_references
    Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 504–510

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles. · source_derived_draft · unverified_draft

    ## silica-nanoparticle-nlrp3 A nanoparticle preparation was examined separately from quartz. Silica nanoparticles increased inflammasome/pyroptosis-associated markers; MCC950 suppressed the response. Model: Mouse RAW-ASC cells; LPS priming, 100 micrograms/mL silica, approximately 30 nm particles. Limitations: Do not assume all sizes, coatings or amorphous preparations behave identically. Evidence access: Primary full text Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
    Complete structured claim and evidence

  3. 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

  4. 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

  5. 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.

    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