Air pollutants include toxic particles and gases emitted in large quantities from many different combustible materials. They also include particulate matter (PM) and ozone, and biological contaminants, such as viruses and bacteria, which can penetrate the human airway and reach the bloodstream, triggering airway inflammation, dysfunction, and fibrosis. Pollutants that accumulate in the lungs exacerbate symptoms of respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Asthma, a heterogeneous disease with complex pathological mechanisms, is characterized by particular symptoms such as shortness of breath, a tight chest, coughing, and wheezing. Patients with COPD often experience exacerbations and worsening of symptoms, which may result in hospitalization and disease progression. PM varies in terms of composition, and can include solid and liquid particles of various sizes. PM concentrations are higher in urban areas. Ozone is one of the most toxic photochemical air pollutants. In general, air pollution decreases quality of life and life expectancy. It exacerbates acute and chronic respiratory symptoms in patients with chronic airway diseases, and increases the morbidity and risk of hospitalization associated with respiratory diseases. However, the mechanisms underlying these effects remain unclear. Therefore, we reviewed the impact of air pollutants on airway diseases such as asthma and COPD, focusing on their underlying mechanisms.

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Background Asthma is diagnosed based on a history of the characteristic symptoms and evidence of expiratory airflow limitation. However, asthma diagnosis using the existing tests is associated with a risk of coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 spread. In this study, we developed a quantitative real‐time polymerase chain reaction (qRT‐PCR)‐based asthma diagnosis tool. Methods We detected nectin‐4 in the plasma of patients with asthma using qRT‐PCR, explored the relationship of clinical variables. Results quantitative real‐time polymerase chain reaction revealed that plasma nectin‐4 mRNA levels were higher in asthmatics than controls. These results correlated with lung function. Conclusions Those results suggest that qRT‐PCR for nectin‐4 may aid asthma diagnosis and monitoring.

and profilin-1 expression in lung microvascular endothelial cells exposed to titanium dioxide nanoparticles [published online as ahead of print on August 24, 2022].

Purpose Junctional adhesion molecule (JAM)-A is an immunoglobulin-like molecule that colocalizes with tight junctions (TJs) in the endothelium and epithelium. It is also found in blood leukocytes and platelets. The biological significance of JAM-A in asthma, as well as its clinical potential as a therapeutic target, are not well understood. The aim of this study was to elucidate the role of JAM-A in a mouse model of asthma, and to determine blood levels of JAM-A in asthmatic patients. Materials and Methods Mice sensitized and challenged with ovalbumin (OVA) or saline were used to investigate the role of JAM-A in the pathogenesis of bronchial asthma. In addition, JAM-A levels were measured in the plasma of asthmatic patients and healthy controls. The relationships between JAM-A and clinical variables in patients with asthma were also examined. Results Plasma JAM-A levels were higher in asthma patients (n=19) than in healthy controls (n=12). In asthma patients, the JAM-A levels correlated with forced expiratory volume in 1 second (FEV 1 %), FEV 1 /forced vital capacity (FVC), and the blood lymphocyte proportion. JAM-A, phospho-JNK, and phospho-ERK protein expressions in lung tissue were significantly higher in OVA/OVA mice than in control mice. In human bronchial epithelial cells treated with house dust mite extracts for 4 h, 8 h, and 24 h, the JAM-A, phospho-JNK, and phospho-ERK expressions were increased, as shown by Western blotting, while the transepithelial electrical resistance was reduced. Conclusion These results suggest that JAM-A is involved in the pathogenesis of asthma, and may be a marker for asthma.

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Objectives: Erdosteine, an oral mucoactive anti-oxidant molecule, interferes with the pathological processes seen in respiratory disorders including thickened or increased mucus production, increased oxidative stress, and chronic inflammation; however, its efficacy as an asthma therapy remains to be fully clarified. Therefore, the aim of this study was to assess the effects of erdosteine on epithelial barrier function in asthma. Methods: To investigate the effects of erdosteine on cell barrier expression in a mouse model of asthma, BALB/c mice ( n = 8 per group; total of 40 mice) were exposed to saline (Sham), ovalbumin (OVA), or OVA plus TiO2 inhalation (200 μg/m3; OVA + TiO2). The mice were then treated with erdosteine orally (OVA + TiO2 + Erdos) or intraperitoneal dexamethasone (OVA + TiO2 + Dex). Bronchoalveolar lavage and histology were performed. Enhanced pause was used as an indicator of pulmonary function, and samples were collected. The effect of erdosteine on cell barrier expression was assessed by immunoblotting and immunohistochemical analyses. Results: OVA + TiO2 + erdosteine mice exhibited decreased inflammation, and mucous gland hyperplasia, and increased pulmonary function compared with OVA + TiO2 mice. Levels of claudin (CLDN)-4 and nectin-4 protein were higher in lung tissue from OVA + TiO2 mice than Sham and OVA mice, and were reduced by erdosteine treatment. In contrast, CLDN14 and CLDN18 protein levels were lower in lung tissue from OVA + TiO2 mice than those from control mice, but were increased by treatment with erdosteine. Conclusion: Cell barriers are involved in airway inflammation in asthma patients, and erdosteine reduces airway inflammation by changing the cell barrier.