Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

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 (FEV1%), FEV1/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 JAMA, 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.