ArticleScientific reports2025
Coal dust particles can upregulate the expression of NLRP3 inflammasome components in rat alveolar macrophages through phagocytosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Research on the Prediction of Coal Workers' Pneumoconiosis Based on Easily Detectable Clinical Data: Machine Learning Model Development and Validation Study.JMIR medical informatics · 2026Article
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- Proteomics-driven screening of artemisinin-based combination ratios and mechanistic insights intoFrontiers in immunology · 2025Article
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7 authors.
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Abstract
Previous studies have demonstrated that silica can activate the NLRP3 inflammasome, and that macrophage phagocytosis is an essential step in this process. Although carbon is the primary component of coal dust particles, it also contains other impurities such as free silica, clay, sulfides, and carbonate minerals. Additional research is still necessary to discover if NLRP3 can be triggered due to the low silica content of coal dust particles. The purpose of this study is to investigate whether coal dust particles can induce the translation and transcription of NLRP3 inflammasome components in rat alveolar macrophages (NR8383) and whether Cytochalasin B may inhibit this process. According to the findings of our research, coal dust particles can upregulate the NLRP3 inflammasome components and IL-1β, a downstream inflammatory component. Furthermore, LPS and coal dust particles work in concert to raise the NLRP3 inflammasome components protein and transcript level in macrophages. Interestingly, the protein and transcript level of NLRP3 inflammasome components dramatically dropped when cells were concomitantly exposed to the actin polymerization inhibitor Cytochalasin B. This suggests that cellular uptake is required for coal dust particles to exert their pro-inflammatory effect.
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