We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics aggravate house dust mite induced allergic airway inflammation through EGFR/ERK-dependent lung epithelial barrier dysfunction
AI summary Read the abstract
In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
Concerns that airborne micro- and nanoplastics (MNPs) may impair human respiratory health are rising. However, the specific effects of MNPs on allergic asthma remain insufficiently explored. This study developed an allergic asthma model using house dust mite (HDM), and mice were exposed to 50 μg polystyrene nanoparticles (PS-NPs) at three-days interval. Additionally, the effects and potential mechanisms of PS-NPs exposure (25, 50 and 100 μg/mL) on lung epithelial barrier dysfunction were explored using mouse lung epithelial type II (MLE-12) and A549 cells. The pathological changes of airway tissue and the increase of inflammatory response confirmed that exposure to PS-NPs significantly aggravated allergic asthma in mice. Importantly, in the presence of HDM sensitization, the accumulation of PS-NPs in the alveolar region was increased, leading to lung epithelial barrier dysfunction and more Th2-mediated eosinophilic inflammation, characterized by elevated IL-4, IL-13, immunoglobulin E (Ig E) and eosinophils. The activation of the epidermal growth factor receptor (EGFR) pathway and its downstream extracellular regulating kinase (ERK) was investigated using transcriptomic sequencing to elucidate the effects of PS-NPs exposure on lung epithelial barrier dysfunction. Furthermore, an EGFR-specific inhibitor AG1478 was employed to confirm the role of the EGFR/ERK pathway in lung epithelial barrier dysfunction and asthma exacerbation in vitro and in vivo experiments. In conclusion, the molecular mechanism by which PS-NPs aggravates asthma in mice was elucidated, which helps to improve the understanding of the health effects of PS-NPs and lays a theoretical foundation for addressing the health risks posed by PS-NPs.
More Papers Like This
Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via CXCL1 signaling pathway in a mouse model
AI summary Read the abstract
In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
Polystyrene nanoplastics impair epithelial barrier establishment and modulate extracellular vesicle release in human bronchial cells cultured at the air-liquid interface
AI summary Read the abstract
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.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
AI summary Read the abstract
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
Polystyrene particles induces asthma-like Th2-mediated lung injury through IL-33 secretion
AI summary Read the abstract
Researchers found that inhaled polystyrene microplastic particles triggered asthma-like inflammation in the lungs of mice, with smaller particles causing more severe responses. The particles stimulated the release of IL-33, a signaling molecule that activates a specific type of immune response associated with allergic airway disease. The study identifies a potential mechanism by which airborne microplastics could contribute to respiratory inflammation.
Co-exposure to microplastics enhances the allergenic potentials of house dust mite allergen Der p 1
AI summary Read the abstract
This study found that polystyrene microplastics can make common house dust mite allergens more potent, increasing allergic reactions. The microplastics changed the shape of the allergen protein, boosting its ability to trigger immune responses and worsening airway inflammation in mice. This research suggests that indoor microplastic pollution could be contributing to the rising rates of allergies and asthma by making existing allergens more harmful.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.