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Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM_2.5)-primed macrophages.

ABSTRACT: Exposure to air pollution fine particulate matter (PM_2.5) aggravates respiratory and cardiovascular diseases. It has been proposed that PM_2.5 uptake by alveolar macrophages promotes local inflammation that ignites a systemic response, but precise underlying mechanisms remain unclear. Here, we demonstrate that PM_2.5 phagocytosis leads to NLRP3 inflammasome activation and subsequent release of the pro-inflammatory master cytokine IL-1β. Inflammasome priming and assembly was time- and dose-dependent in inflammasome-reporter THP-1-ASC-GFP cells, and consistent across PM_2.5 samples of variable chemical composition. While inflammasome activation was promoted by different PM_2.5 surrogates, significant IL-1β release could only be observed afte

SUBMITTER: Caceres L

PROVIDER: S-EPMC10804998 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Dataset Information

Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM_2.5)-primed macrophages.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM2.5)-primed macrophages.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM_2.5)-primed macrophages.