The migration of eosinophils and lymphocytes into airways is a hallmark of allergic asthma; however, the role of broncho-alveolar macrophages (BAMs) in this inflammatory process has not been fully elucidated. Using a murine Ova model of allergic airway disease (AAD), RNA isolated from BAMs was used to assess differential gene expression via microarray and qRT-PCR. Significant increases in WBCs, eosinophilia, mucus accumulation and goblet cell hyperplasia were observed in Ova sensitized and challenged mice, which correlated with increased expression of genes associated with alternatively activated M2 macrophages (e.g. arginase 1, YM-1, YM-2, Resistin like-α, and EAR-11). Other genes associated with asthma including FcγRIIb, MMP-14, CCL-8, CCL-17, ADAM-8, LTBR1, aquaporin-9 and IL-7R were also expressed at higher levels in Ova sensitized/challenged animals when compared to BAMs isolated from control animals. Eotaxin 2 (CCL-24), which is known to influence eosinophil migration, was highly up-regulated in BAMs, but not Eotaxin-1 (CCL-11). Conversely, lung interstitial macrophages expressed high levels of CCL-11, but not CCL-24. Taken together, this study provides additional evidence to support the notion that M2 BAMs play a role in eosinophil and potentially other leukocyte migration patterns into asthmatic airways.
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