Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via IL-8 signaling pathway in a mouse model of asthma
Description
Background: Environmental pollutants have been found to contribute to the development and acute exacerbation of asthma. Microplastics 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 the following four groups: (i) Control group, treated only with PBS; (ii) MP group, exposed to PE-MPs and PBS; (iii) Asthma group, sensitized and challenged with HDM; (iv) Asthma+MP group, asthma group intranasally exposed to 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 more inflammatory cell, bronchial goblet cell hyperplasia, collagen deposition, allergen sensitization, and Th2 immune bias than HDM-sensitized mice without PE-MPs treatment. PE-MPs and HDM co-exposure aggravated oxidative stress injury in the lung. The production of airway-derived cytokine IL-33 was also increased in the BALF of mice co-exposed to PE-MPs and HDM. In addition, co-exposure to PE-MPs and HDM reduced the integrity and the expression of relevant molecules of the airway epithelial barrier. Lung tissue transcriptomics analysis revealed that PE-MPs exposure was associated with IL-8 signaling and neutrophil activation in asthmatic mice.