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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
Summary
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.
BACKGROUND: Environmental pollutants have been found to contribute to the development and acute exacerbation of asthma. Microplastics (MPs) have received widespread attention as an emerging global pollutant. Airborne MPs can cause various adverse health effects. Due to their hydrophobicity, MPs can act as a carrier for other pollutants, pathogens, and allergens. This carrier effect of MPs may adsorb allergens and thus make the body exposed to MPs and a large number of allergens simultaneously. We hypothesized that co-exposure to inhaled MPs and aeroallergens may promote the development of airway inflammation of asthma by disrupting the airway epithelial barrier. METHODS: The effects of co-exposure to Polyethylene microplastics (PE-MPs) and allergens on allergic airway inflammation and airway epithelial barrier were examined in a mouse model of asthma. The mice were divided into four groups: (i) Control group, treated only with PBS; (ii) MP group, exposed to PE-MPs and PBS; (iii) HDM group, mice were sensitized and challenged with HDM, and intranasally treated with PBS; (iv) HDM + MP group, mice were sensitized and challenged with HDM, and intranasally treated with PE-MPs. Histology and ELISA assays were used to evaluate the severity of airway inflammation. FITC-dextran permeability assay, immunofluorescence assay, and RT-PCR were used to evaluate the airway epithelial barrier function and the expression of relevant molecules. Transcriptomics analysis with lung tissue sequencing was conducted to identify possible pathways responsible for the effects of PE-MPs. RESULTS: Co-exposure of mice to PE-MPs and HDM induced a higher degree of inflammatory cell infiltration, bronchial goblet cell hyperplasia, collagen deposition, allergen sensitization, and Th2 immune bias than exposure to HDM alone. Co-exposure to PE-MPs and HDM aggravated oxidative stress injury in the lung and the production of cytokine IL-33 in the BALF. In addition, co-exposure of mice to PE-MPs and HDM resulted in a more pronounced decrease in the expression of relevant molecules of the airway epithelial barrier and more significant increase in the permeability of airway epithelia. Lung tissue transcriptomics analysis revealed that PE-MPs exposure was associated with CXCL1 signaling and neutrophil activation. CONCLUSION: Co-exposure to MPs and HDM may promote airway inflammation and airway epithelial barrier disruption and induce immune responses characterized by CXCL1 signaling and neutrophilic inflammation.
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