Abstract: Objective：To explore the role of exposure to PM2.5 on Th9 cell differentiation and its role in the pathology of asthma to provide evidence for causal relationship between air pollution and asthma and to find new treatment strategy for asthma. Methods：Mice were sensitized and challenged with cockroach extract (CRE) by intratracheal inhalation. Different dose of PM2.5 were inhaled by intratracheal injection during the challenging period. Cell counting in the bronchoalveolar lavage fluid (BALF), HE staining of lung tissues and resistance of airway were detected to evaluate the effect of PM2.5 on asthma. Th9 cells in the lung hilar lymphnodes was detected with flow cytometry. IL-9 expression in the lung tissues was detected with qRT-PCR. Th9 cells were differentiated in the presence of IL-4 and TGF-β with naive CD4+ T cells in vitro. IL-9，PU.1 and BATF were detected with qRT-PCR or flow cytometry. Results：The lung inflammation were significant enhanced in the PM2.5 together with allergen (CRE) group compared with CRE group. The total cell numbers, the number of eosinophils, granulocytes and lymphocytes in the BALF, lung inflammation, and airway resistance were significant increased in the PM2.5+CRE group compared with CRE group. There was more Th9 positive cells in lung hilar lymphonodes in the PM2.5+CRE group than CRE group. The IL-9 positive cells was more in the PM2.5+CRE group than CRE group in in-vitro experiment (52.0%±5.8% vs 31.7%±3.2%, P=0.000 4 ). PU.1 and BATF expression was also higher in the PM2.5+CRE group than CRE group. Conclusion：PM2.5 could enhance the inflammation of asthma and this may be related to its effect on Th9 cells differentiation.