ArticleBMC biology2025
Cholesterol-mediated inflammation activation in alveolar macrophages.
Article in BMC biology, 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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Who cites it
3 citing papers in PubMed.
- NLRP3 inflammasome activation by particles and fibers: implications for human hazard assessment.Archives of toxicology · 2026Review
- Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics.Frontiers in immunology · 2026Review
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
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3 authors.
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Abstract
backgroundThe role of cholesterol- and cholesterol crystal-mediated inflammation has been extensively investigated in circulating macrophages in the context of cardiovascular diseases while little is known about its contribution to lung diseases. However, lipid-laden alveolar macrophages and crystal-like structures have been reported in lungs of different human and animal models of lung diseases. In this study, we address the hypothesis that a mechanism of inflammasome activation, due to altered cholesterol metabolism, may occur also in alveolar macrophages.
resultsWe tested the effect of soluble (cholesterol-enriched liposomes) and crystalized cholesterol exposure in a cell model of macrophages and in primary murine alveolar macrophages. Both soluble and crystalized cholesterol can be taken up by macrophages, mainly by phagocytosis for the crystals. Prolonged exposure to both forms of cholesterol leads to intracellular cholesterol accumulation in cytoplasmic lipid droplets and to foam cell formation in a time-dependent manner. However, in unprimed alveolar macrophages, immunofluorescence detection of the NLRP3 inflammasome and analysis of inflammatory cytokines showed that only cholesterol crystals stimulate the assembly of the inflammasome in speck and release of IL-18, indicating the sterile activation of the inflammasome. The role of NLRP3 was confirmed by chemical inhibition of the NLRP3 inflammasome in vitro and by validation in macrophages from NLRP3-deficient mice.
conclusionsIn alveolar macrophages, cholesterol crystals, but not soluble cholesterol, trigger the assembly and activation of the inflammasome, thus leading to the inflammasome-dependent release of IL-18. These results open new scenarios for the role of alveolar macrophages and of cholesterol-mediated inflammation in the lung.
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