Component
Mouse MARCO
Context-specific entity; species, compartment and exposure are stated on each claim.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake.
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 evidenceMARCO loss or antibody blockade prevented silica uptake and cytotoxicity in C57BL/6 alveolar macrophages.
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
Where it participates (unsigned role)
U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.