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Epidemiological studies have reported that elevated ambient particulate matter (PM) concentrations are associated with exacerbations of asthma.To determine the underlying mechanism, we combined asthma mice model with PM instillation.PM (collected in Nanjing in 2014), PBS or control filters extracts (CSF) were administered to OVA-sensitized mice before OVA challenge.In asthmatic mice, compared with PBS or CSF instillation, PM and OVA coexposure showed enhanced airway hyperresponsiveness , increased lung infiltration with eosinophils and macrophages, incresed OVA-specific IgE in serum and increased cytokine levels including IL4, IL13, eotaxinl in bronchoalveolar lavage and lung tissue homogenate supernatant.Confocal fluorescence microscopy revealed eotaxinl which is crucial in eosinophils recruitment is mainly localized to CD68-positive macrophages.In the Th2 cytokine immune microenvironment, both alveolar and interstitial macrophages in asthmatic mice are alternative activated with significant upregulation of M2 polarization markers arginase-1, CD206, YM1/2.By contrast, YM1/2 expression in lung tissue of PM and OVA coexposure group is further elevated, which implies more M2 macrophage infiltration.BMDM were isolated and polarized to M2 macrophage with IL-4/IL-13.Then M2 macrophages were adoptively transferred into allergic mice after last OVA challenge, elevated the percentage of CD11b+Siglec+ eosinophils in lung of asthmatic mice were detected in a number dependent manner.In vitro, PM was administered to bone marrow derived macrophage (BMDM) directly , but no significant changes in M2 makers were found.M2 macrophage was induced by stimulating BMDM with IL4/IL13, which has significant up regulation of eotaxin1.Taken together, our results suggested that PM could synergize with allergens to aggravate the severity of asthma, and additional eotaxinl released from M2 macrophage might respond for the increased eosinophils infiltration.