ArticleJournal of immunology research2014
Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO.
Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Inorganic Arsenic Attenuates Crystalline Silica-Induced Pulmonary Inflammation and Fibrosis by Ameliorating Autophagolysosomal Dysfunction in Alveolar Macrophages.Biological trace element research · 2026Article
- A comprehensive retrospect on the current perspectives and future prospects of pneumoconiosis.Frontiers in public health · 2024Review
- Cholesterol-dependent molecular mechanisms contribute to cationic amphiphilic drugs' prevention of silica-induced inflammation.European journal of cell biology · 2023Article
- Self-replicating murine ex vivo cultured alveolar macrophages as a model for toxicological studies of particle-induced inflammation.Toxicology and applied pharmacology · 2023Article
- Cholesterol content regulates silica-induced lysosomal membrane permeability.Frontiers in toxicology · 2023Article
- Preclinical Mouse Model of Silicosis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Nicotine exacerbates atherosclerosis and plaque instability via NLRP3 inflammasome activation in vascular smooth muscle cells.Theranostics · 2023Article
- Contribution of Particle-Induced Lysosomal Membrane Hyperpolarization to Lysosomal Membrane Permeabilization.International journal of molecular sciences · 2021Article
- Omega-3 Polyunsaturated Fatty Acid Intervention Against Established Autoimmunity in a Murine Model of Toxicant-Triggered Lupus.Frontiers in immunology · 2021Article
- Article
- Silica exposure and chronic virus infection synergistically promote lupus-like systemic autoimmunity in mice with low genetic predisposition.Clinical immunology (Orlando, Fla.) · 2019Article
- Prevention of crystalline silica-induced inflammation by the anti-malarial hydroxychloroquine.Inhalation toxicology · 2019Article
- Crosstalk Between Acid Sphingomyelinase and Inflammasome Signaling and Their Emerging Roles in Tissue Injury and Fibrosis.Frontiers in cell and developmental biology · 2019Review
- Imipramine blocks acute silicosis in a mouse model.Particle and fibre toxicology · 2017Article
- Phagolysosome acidification is required for silica and engineered nanoparticle-induced lysosome membrane permeabilization and resultant NLRP3 inflammasome activity.Toxicology and applied pharmacology · 2017Article
- Volcanic Ash Activates the NLRP3 Inflammasome in Murine and Human Macrophages.Frontiers in immunology · 2017Article
- Autophagy deficiency in macrophages enhances NLRP3 inflammasome activity and chronic lung disease following silica exposure.Toxicology and applied pharmacology · 2016Article
- The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases.Particle and fibre toxicology · 2016Review
- Cell-Based Therapy for Silicosis.Stem cells international · 2016Review
- Silica-Triggered Autoimmunity in Lupus-Prone Mice Blocked by Docosahexaenoic Acid Consumption.PloS one · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
MARCO is the predominant scavenger receptor for recognition and binding of silica particles by alveolar macrophages (AM). Previously, it was shown that mice null for MARCO have a greater inflammatory response to silica, but the mechanism was not described. The aim of this study was to determine the relationship between MARCO and NLRP3 inflammasome activity. Silica increased NLRP3 inflammasome activation and release of the proinflammatory cytokine, IL-1β, to a greater extent in MARCO(-/-) AM compared to wild type (WT) AM. Furthermore, in MARCO(-/-) AM there was greater cathepsin B release from phagolysosomes, Caspase-1 activation, and acid sphingomyelinase activity compared to WT AM, supporting the critical role played by lysosomal membrane permeabilization (LMP) in triggering silica-induced inflammation. The difference in sensitivity to LMP appears to be in cholesterol recycling since increasing cholesterol in AM by treatment with U18666A decreased silica-induced NLRP3 inflammasome activation, and cells lacking MARCO were less able to sequester cholesterol following silica treatment. Taken together, these results demonstrate that MARCO contributes to normal cholesterol uptake in macrophages; therefore, in the absence of MARCO, macrophages are more susceptible to a greater inflammatory response by particulates known to cause NLRP3 inflammasome activation and the effect is due to increased LMP.
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