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Polystyrene microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils
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Researchers orally administered 1 μm and 10 μm polystyrene particles to mice for 10 days and found that both sizes crossed the intestinal epithelium and were detected in blood and liver; when phagocytosed by human monocytes and neutrophils, the particles triggered complement-dependent inflammatory cell death.
Microplastics have been detected in human blood, raising concerns about human health. Here, we investigated the tissue distribution of microplastics after oral exposure in mice and their effects on mouse and human phagocytes. Both 1 and 10 μm polystyrene (PS) particles crossed the intestinal epithelium and were detected in the blood and liver of mice after ten days of oral administration. Intravital microscopy visualized phagocytosis of 1 μm PS by mouse neutrophils in the liver. Phagocytosis by human neutrophils required plasma or serum-coating of PS and was complement-dependent. Phagocytosis of coated PS induced monocyte and neutrophil cell death, with 10 μm PS requiring a single particle uptake, whereas 1 μm PS required much higher exposure levels. Neutrophil cell death upon 10 μm PS phagocytosis was characterized by extracellular DNA and classified as NETosis. These findings demonstrate that microplastics can penetrate tissues and provoke pro-inflammatory immune cell death, suggesting potential risks to human health.
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Microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils
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Researchers administered polystyrene microplastics orally to mice and then assessed distribution and immune cell interactions in both mice and human cells. Both 1 µm and 10 µm particles crossed the intestinal epithelium and were detected in blood and liver after 10 days, and human monocytes and neutrophils that ingested the particles underwent inflammatory cell death.
Ingestion of micro- and nanoplastic perturbs tissue homeostasis and macrophage core functions
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Researchers fed mice polystyrene particles chronically and found that micro- and nanoplastics breached intestinal barriers and accumulated in multiple organs, disrupting tissue homeostasis and impairing core macrophage functions including phagocytosis and inflammatory regulation.
Noxic effects of polystyrene microparticles on murine macrophages and epithelial cells
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Polystyrene microparticles induced cytotoxic effects in murine macrophages and intestinal epithelial cells at higher concentrations, triggering cell membrane damage, inflammatory cytokine release, and reduced phagocytic function, with smaller particles generally causing greater harm than larger ones at equivalent mass doses.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
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Researchers exposed colitis mouse models to polystyrene micro- and nanoplastics to test whether MNP exposure worsens inflammatory bowel disease, finding that MNPs altered biodistribution and exacerbated inflammatory responses in animals with pre-existing gut inflammation.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
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Researchers induced colitis in mice using dextran sodium sulfate and orally administered polystyrene micro- and nanoplastics of three sizes, then tracked biodistribution, macrophage polarization, and gut microbiome changes. In colitis conditions, microplastic uptake into systemic tissues was enhanced, macrophages shifted toward a pro-inflammatory phenotype, and gut microbial diversity decreased, suggesting that inflammatory bowel disease increases vulnerability to microplastic-driven systemic harm.
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