Objective:To observe the effects of fine particulate matter (PM2.5) by different dosages at short-term exposure on airway inflammation in asthmatic mice, and study the mechanisms of PM2.5 on airway inflammation in asthmatic mice. Methods: A total of 40 BALB/c mice were randomly assigned into 5 groups, including the PBS control group, the OVA group (asthma group), the OVA PM2.5 (10 μg) group, the OVA PM2.5 (31.6 μg) group,and the OVA PM2.5 (100 μg) group. Asthma model was reproduced by sensitization with intraperitoneal injection and inhalation of OVA. On day 26, 28 and 30, the mice were performed with PM2.5 intranasal stimulation, and then sacrificed on day 31. We observed the pathological changes and inflammatory cell infiltration by hematoxylin-eosin (HE) staining of lung tissues of mice alveolar fluid (BALF) cells in each group. IL-4/IL-13 and serum IgE levels were examined by the method of ELISA. Results: Compared with the asthma group, the differences in cell count and levels of IL-4/IL-13 were not statistically significant in the PM2.5 (10 μg)/OVA group(P > 0.05), while those in the PM2.5(31.6 μg)/OVA group and the PM2.5(100 μg)/OVA group were increased (P < 0.05). The level of serum IgE in the PM2.5 (10 μg)/OVA group and the PM2.5 (31.6 μg)/OVA group was increased slightly compared with the OVA group, but there was no significant difference(P > 0.05). However, the level of serum IgE in the PM2.5(100 μg)/OVA group was significantly increased than that of the OVA group(P < 0.05). Conclusion: The asthma airway inflammation may further aggravate in the PM2.5(31.6 μg)/OVA and PM2.5 (100 μg)/OVA, and no significant effect was from the PM2.5 (10 μg)/OVA.