Background: Tyrosine phosphorylation of MUC1 CT domain leads to inhibition of TLR signaling and down-regulation of inflammation. We tested, the expression of Muc1 gene in OZONE induced airway injury using animal models. Methods: The mice housed in whole-body exposure chambers were exposed to ozone concentrations of 2 ppm for 3 h (n=6) daily. After measurements of differential cell count were done in bronchoalveolar lavage (BAL) fluid, MUC1and proliferating cell nuclear antigen (PCNA) protein expression were observed in lung tissue using immunohistochemical stain (IHC). Results: 1. 3 weeks OZONE exposure increased the numbers of total cells, and neutrophils in BAL fluids of OZONE- sensitized/challenged mice in a time -dependent manner (P＜0.05). But, on 14th days, the total cells and neutrophils were decreased again in 1weeks OZONE exposure mice. 2. MUC1 expressions were decreased in the 3 weeks OZONE exposure mice in a time -dependent manner (P＜0.05). PCNA expressions were significantly increased in the 3 weeks OZONE exposure mice in a time -dependent manner until 14th days (P＜0.05). 3. 1 weeks OZONE exposure were decreased in a time -dependent manner (P＜0.05). But it was increased again after 14th days. PCNA expressions were increased in the OZONE exposure mice in a time -dependent manner until 7th days. But, with decreased after 14th days (P＜0.05). Conclusions: These results indicate that MUC1 expressions by ozone were decreased, and this may lead to excessive airway inflammation.