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Gasdermin D-dependent macrophage pyroptosis mediates polystyrene microplastics-induced pulmonary fibrosis
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Researchers demonstrated that chronic intranasal exposure to polystyrene microplastics in mice triggered a specific form of inflammatory cell death called pyroptosis in lung macrophages, leading to pulmonary fibrosis. The study identified the Gasdermin D protein as a key mediator of this process, suggesting a potential mechanistic pathway through which microplastic inhalation could contribute to lung tissue scarring.
Exposure to microplastic (MPs) pollution may induce pulmonary fibrosis (PF). Macrophage pyroptosis has been directly implicated in the pathogenesis of PF. This study focused on the potential driving role of macrophage pyroptosis in polystyrene microplastics (PS-MPs) induced pulmonary fibrosis. Through a 56-day intranasal exposure model in mice, we demonstrate that chronic exposure to 5-μm PS-MPs induces significant pulmonary fibrosis characterized by collagen deposition, extracellular matrix remodeling, and substantial lung function impairment. PS-MPs specifically trigger GSDMD-dependent pyroptosis in alveolar macrophages, as evidenced by enhanced NLRP3 inflammasome assembly, caspase-1 activation, and GSDMD-NT pore formation. Genetic ablation of Gsdmd substantially attenuated fibrotic progression, improved pulmonary functional parameters, and reduced production of pro-fibrotic mediators including IL-1β. Crucially, we established a direct paracrine link between macrophage pyroptosis and fibrogenesis through conditioned medium experiments, demonstrating that GSDMD-dependent release of pyroptotic factors promotes fibroblast activation and extracellular matrix production. Our results delineate a complete pathogenic pathway wherein PS-MPs induce pulmonary fibrosis through macrophage pyroptosis, thereby positioning GSDMD as both a key mediator and promising therapeutic target for combating microplastic-associated lung disease. These findings provide crucial insights into the environmental health risks of microplastics and identify potential intervention strategies for plastic pollution-related respiratory disorders.
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Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
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Researchers found that mice exposed to polystyrene microplastics through their noses developed lung scarring (fibrosis) because the plastic particles triggered a form of cell death called ferroptosis, involving iron buildup and cell damage in lung tissue. Blocking the specific signaling pathway responsible (cGAS/STING) reduced the lung damage, pointing to a potential treatment approach if microplastic-related lung disease becomes a clinical concern.
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
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Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Nasal instillation of polystyrene nanoplastics induce lung injury via mitochondrial DNA release and activation of the cyclic GMP-AMP synthase-stimulator of interferon genes-signaling cascade
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Researchers showed that inhaled polystyrene nanoplastics trigger lung fibrosis and inflammation in mice by inducing mitochondrial DNA release into the cytoplasm, which activates the cGAS-STING innate immune signaling pathway — a discovery that identifies a specific molecular mechanism linking nanoplastic inhalation to pulmonary injury.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
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Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
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