Background: Air pollutants induce or incite respiratory diseases such as asthma and COPD. Whether junctional proteins can contribute to development or exacerbations of airway diseases remain to be clarified. Objective: The aim of this study was to observe the effect of diesel exhaust particulates (DEP) on junctional proteins of both nose and lung in a mouse model. Methods: Mice were treatment with saline (Sham) and exposed to 100 μg/m3 DEPs 1 hour a day for 5 days a week for 4 weeks and 8 weeks in a closed-system chamber attached to a ultrasonic nebulizer. Airway hyperresponsiveness (AHR) was measured and bronchoalveolar lavage fluid, lung and nasal tissue were collected. The effects of DEP on junctional proteins such as claudin (CLND) 4, CLND 5, and CLND 17 were estimated using Western blot, immunohistochemical stain in nasal and lung tissue. Results: AHR and inflammatory cells in the airway were higher in DEP exposure group than in control group and were higher in 4 and 8 weeks group than in control group. The expression of CLND4, CLND 5, and CLND 17 in both lung and nasal tissue were significantly increased in DEP exposure group than in the control group. Conclusion: These results suggesting that air pollutants can change CLDNs and disintegrate cell barriers, causing to airway inflammation of both nose and lung.