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Integrin A5B1-mediated endocytosis of polystyrene nanoplastics: Implications for human lung disease and therapeutic targets
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This study identified a specific protein, integrin alpha-5-beta-1, as a key gateway that allows polystyrene nanoplastics to enter human lung cells. Once inside, the nanoplastics triggered inflammation, oxidative stress, and cell damage that could contribute to respiratory disease and lung cancer risk. The discovery of this entry mechanism could provide a potential drug target for reducing the harmful effects of inhaled nanoplastics on lung health.
The extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5β1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5β1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5β1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases.
More Papers Like This
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
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Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Endocytosis, Distribution, and Exocytosis of Polystyrene Nanoparticles in Human Lung Cells
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Researchers studied how polystyrene nanoparticles of 50 and 100 nanometers enter and exit human lung cells. They found that cellular uptake increased with exposure time and dose, with the smaller particles being taken up more readily and primarily accumulating in lysosomes. The study reveals that while lung cells can expel some ingested nanoplastics, a significant portion remains inside the cells, raising concerns about long-term respiratory exposure.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
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Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Polystyrene nanoplastics impair epithelial barrier establishment and modulate extracellular vesicle release in human bronchial cells cultured at the air-liquid interface
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Scientists exposed lab-grown human airway cells to tiny nanoplastic particles (like those found in breathing air polluted with plastic waste) and found the particles weakened the protective barrier these cells normally form, while also triggering inflammation-related signals. This suggests nanoplastics could make airways more vulnerable, especially in people whose lung lining is already damaged or still developing—though this was shown in a lab model, not in humans breathing polluted air, so more research is needed to confirm real-world impact.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
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Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
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