So far, epidemiological data have revealed that the elevation of fine ambient particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) is closely associated with an exacerbation of asthma while the underlying mechanism is poorly understood. Using a murine model, we investigated the impact of PM2.5 on the development of asthma. Before OVA challenge, mice were administrated with PM2.5, phosphate-buffer saline (PBS) or control filter extracts (CFE). Results showed that compared to PBS or CSF, PM2.5 co-exposure with OVA led to a higher airway hyperresponsiveness (AHR) and a severer eosinophils infiltration. Both alveolar and interstitial macrophages are alternatively activated in OVA-challenged mice with a propensity to M2, marked by arginase-1, CD206, and YM-1. PM2.5 co-exposure dramatically elicited a YM-1 upregulation, implying an aggravated M2 polarization and macrophages recruitment. Eotaxin-1 was predominantly detected in YM-1-positive macrophages, and the level as well as those of IgE, IL-4 or IL-13 was notably increased by PM2.5 co-exposure. With IL-4/IL-13-induced transformation of bone marrow-derived macrophages (BMDM), these M2-polarized macrophages were adoptively transferred into allergic mice. An increase of CD11b+ Siglec+eosinophils was observed in these mice while in vitro, no significant polarization of BMDM was found when treated with PM2.5. Together, our findings suggested that PM2.5 could exacerbate asthma by aggravating M2-polarization, highlighting for the first time that Eotaxin-1 released from M2 macrophages plays a crucial role in asthma pathogenesis.