Epithelial barrier dysfunction is involved in allergic inflammation and asthma, due to increased exposure of sub-epithelial tissues to inhaled allergens and air pollutants. The tight junction proteins claudins (CLDNs) are important regulators of paracellular permeability. CLDN7 is expressed in the alveolar epithelium; however, its contribution to airway barrier function remains unclear. The aim of this study was to assess the effects of TiO on epithelial barrier function in asthma. Mice were sensitized and challenged with OVA or exposed to TiO on days 21-23. The effect of TiO on CLDN7 was assessed by ELISA, immunoblotting, and immunohistochemical analysis. The levels of CLDN7 in the plasma of patients with asthma and healthy individuals were also examined. CLDN7 levels were lower in plasma from patients with asthma compared with healthy individuals. CLDN7 levels were associated with FEV/FVC and the blood eosinophils (%) in patients with asthma. Although CLDN7 expression was elevated in the lungs of mice with asthma and in NHBE cells treated with HDM extracts, its expression was suppressed by exposure to TiO. p-AKT and p-ERK was increased in asthmatic mice and decreased in mice with TiO treatment. p-AKT and p-ERK was decreased in NHBE cells treated with TiO and HDM extracts. Trans-epithelial electrical resistance (TEER) was higher in NHBE cells treated with TiO or HDM extracts; however, this was decreased by concurrent TiO and HDM extracts treatment. Our data suggest that particulate matter contributes to airway epithelial barrier dysfunction and results in airway inflammation and responsiveness.

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