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- W622335006 abstract "Abstract In healthy lungs, alveolar macrophages comprise >95% of the immune cells in the alveolar airspaces where they regulate local lung surfactant production and act as the primary sentinels of respiratory pathogens. Interestingly, increased AMΦ numbers are observed in many animal models of chronic lung diseases and also clinically in patients with COPD. Combining flow cytometry and chimeric mice studies, we observed that residential AMΦs form two distinct subpopulations (by either remaining Mac-1neg/low or turning Mac-1pos) during acute inflammation and in chronic inflammatory lung disease subsequent to SHIP-1 deletion. SHIP-1-/- mice which spontaneously develop COPD-like lung disease maintain both Mac-1neg/low and Mac-1pos AMΦ subpopulations. This additional Mac-1pos subpopulation highly expresses MMP-12 and tracks with the induction of lung disease using SHIP-1-/- chimeric mice. Altogether, our results suggest that residential AMΦ heterogeneity is a component of acute lung inflammation and chronic inflammatory lung disease. Consequently, whether residential AMΦ heterogeneity may be a novel hallmark of inflammation-driven human lung diseases has been our final area of study. Overall, our studies of both animal models and patient samples may allow us to better understand the role of AMΦ heterogeneity in lung homeostasis and disease." @default.
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- W622335006 date "2013-05-01" @default.
- W622335006 modified "2023-09-26" @default.
- W622335006 title "Delineating residential macrophage heterogeneity in lung disease (P3282)" @default.
- W622335006 doi "https://doi.org/10.4049/jimmunol.190.supp.136.23" @default.
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