European Respiratory Society

Figure 2.

Fri, 2021-07-09 17:29 -- admin
Silica-induced activation of inflammasome and interleukin (IL)-1 production. IL-1α, released from alveolar macrophages following crystalline exposure, results in NF-κB activation and transcription and translation of pro-IL-1β. Phagocytosis of crystalline silica leads to phagosomal damage and release of the phagosome contents into the cytoplasm. This results in the activation of NALP3 (NACHT, LRR, and PYD domains-containing protein 3) and its association with the intracellular adapter protein ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), which combines with and activates pro-caspase-1. The resulting inflammasome cleaves pro-IL-1β to the pro-inflammatory IL-1β. However, binding of immobilised silica crystals to the cell membrane of macrophages is also sufficient to induce IL-1β without evidence of lysosomal damage. Activation of the NALP3 inflammasome by silica also results in efflux of intracellular potassium ions, suggesting a possible interaction of silica with a membrane-associated protein, but it is unclear whether potassium ion efflux following binding of immobilised silica crystals to the cell membrane results in inflammasome activation. Scavenger receptors have a role in the recognition and uptake of silica. Reproduced with kind permission of Michael Pollard, Scripps Research, San Diego, CA, USA.
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<atom:author xmlns:atom="" xmlns:hwp="" xmlns:nlm="" hwp:inherited="yes" nlm:contrib-type="author"><atom:name>Deborah Helwen Yates</atom:name><atom:email></atom:email><nlm:name name-style="western" hwp:sortable="Yates Deborah Helwen"><nlm:surname>Yates</nlm:surname><nlm:given-names>Deborah Helwen</nlm:given-names></nlm:name></atom:author>
<atom:contributor xmlns:atom="" xmlns:hwp="" xmlns:nlm="" hwp:inherited="yes" nlm:contrib-type="author"><atom:name>Anthony Rutledge Johnson</atom:name><nlm:name name-style="western" hwp:sortable="Johnson Anthony Rutledge"><nlm:surname>Johnson</nlm:surname><nlm:given-names>Anthony Rutledge</nlm:given-names></nlm:name></atom:contributor>
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