Polystyrene microplastic particles induce autophagic cell death in BEAS‐2B human bronchial epithelial cells

Dec 9, 2022Environmental toxicology

Polystyrene microplastic particles cause self-destructive cell death in human lung airway cells

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Abstract

Positively charged polystyrene microplastics (NH-PS-MPs) induced cytotoxicity and increased reactive oxygen species generation in lung cells.

Only NH-PS-MPs showed significant cytotoxic effects and elevated reactive oxygen species in bronchial epithelial cells.
In animal experiments, NH-PS-MPs notably increased the expression and secretion of the pro-inflammatory cytokine IL-1β.
Analysis of ER stress proteins indicated that NH-PS-MPs activated stress pathways associated with cellular damage.
Autophagic cell death and nuclear deformities were observed in lung cells exposed to NH-PS-MPs.
Repeated inhalation of microplastics may lead to inflammatory responses in the lungs due to damage to epithelial cells.

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The detection of high levels of microplastics in indoor and outdoor air has increased concerns regarding its toxic effects on the respiratory system. They are not easily degradable and can be deposited deep in the lungs. Although several studies have reported inhalation toxicities of microplastics, they are still controversial due to a lack of evidence. Herein, we evaluated the inhalation toxicities of three differently charged polystyrene microplastics (PS-MPs), the most abundant microplastics in the air. Cytotoxicity and ROS generation were evaluated using WST-1 and DCF-DA assays, respectively. To evaluate the toxic effects on the lung, inflammatory responses were analyzed after repeated exposure to the PS-MPs through intratracheal instillation. To explore the mechanism of toxicity, autophagy and ER stress-associated proteins were analyzed. Only the positively charged PS-MPs (NH-PS-MPs) showed cytotoxicity and increased ROS generation in BEAS-2B cells. Similarly, only NH-PS-MPs significantly increased the expression and secretion of the pro-inflammatory cytokine IL-β in the animal experiments. The expression of ER stress proteins indicated that NH-PS-MPs increased ER stress via PERK-EIF2α and ATF4-CHOP pathways. Moreover, accumulation of NH-PS-MPs in lysosomes and deformity of the nucleus were observed in BEAS-2B cells with autophagy induction. Taken together, our results demonstrated that NH-PS-MPs induced autophagic cell death in bronchial epithelial cells, leading to inflammatory responses in the lungs. These results suggest that repeated inhalation of microplastics can result in inflammatory responses in the lung through cellular damage of lung epithelial cells, and that inhalation microplastics should be monitored to reduce inhalation health risks. 2 2 2 2 2

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Polystyrene microplastic particles induce autophagic cell death in BEAS‐2B human bronchial epithelial cells

Abstract

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