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Polypropylene Microplastics Disrupt Epithelial Barrier Integrity and Viability in Human Airway Epithelial Cells

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Scientists found that tiny polypropylene microplastic particles, the kind used in many plastic products, can damage the cells lining our airways when exposed in lab experiments. The plastics caused cell stress that weakened the "seals" between cells, making the airway barrier leaky. This suggests breathing in microplastics could potentially harm lung health, though more research is needed to confirm this happens in real life.

Polymers
Body Systems

ObjectiveTo investigate the effects of polypropylene microplastics (PP-MPs) on the integrity and viability of upper airway epithelial cells and to elucidate the underlying mechanisms.MethodsHuman nasal primary epithelial cells and a human alveolar epithelial cell line A549 were exposed to PP-MPs. Intracellular reactive oxygen species (ROS) production, epithelial-mesenchymal transition (EMT) markers (N-cadherin, vimentin), and tight junction (TJ) proteins (ZO-1, E-cadherin, occludin) were analyzed. Activation of the TGF-β/p38 mitogen-activated protein kinase (MAPK) signaling pathway was evaluated. In addition, the effects of the ROS scavenger N-acetyl-L-cysteine (NAC) were assessed.ResultsPP-MP exposure significantly increased intracellular ROS production and induced EMT, as evidenced by upregulation of N-cadherin and vimentin, along with downregulation of TJ proteins, including ZO-1, E-cadherin, and occludin. These changes were associated with activation of the TGF-β/p38 MAPK signaling pathway. NAC treatment effectively reversed these effects, restoring epithelial barrier integrity.ConclusionPP-MPs induce EMT and impair epithelial barrier function through ROS-mediated activation of the TGF-β/p38 MAPK pathway. These findings highlight the potential respiratory health risks associated with MP exposure.

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