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Exposure to Ambient Particles Alters the Evolution of Macrophage Phenotype and Amplifies the Inducible Release of Eotaxin-1 in Allergen-Sensitized Mice.

So far, epidemiological data have revealed that the elevation of fine ambient particulate matter (aerodynamic diameter ≤2.5 μ m; 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.

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