Abstract
Tissue-resident alveolar macrophages (TR-AM) are depleted from the lung during the early stages of bleomycin-induced lung injury and fibrosis. The recovery of the population of macrophages after bleomycin could be completely attributable to the recruitment and differentiation of monocyte-derived alveolar macrophages (Mo-AM). The authors used multiple lineage-trace mouse models where they selectively depleted TR-AM or Mo-AM and induced fibrosis with bleomycin. Deletion of TR-AM had no effect on the severity of the fibrotic phenotype. However, when Mo-AM were depleted animals showed attenuated fibrosis as evidenced by normalised collagen levels and recovered lung compliance.
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