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Joshi, Nikita; Watanabe, Satoshi; Verma, Rohan; Jablonski, Renea P; Chen, Ching-I; Cheresh, Paul; Markov, Nikolay S; Reyfman, Paul A; McQuattie-Pimentel, Alexandra C; Sichizya, Lango; Lu, Ziyan; Piseaux-Aillon, Raul; Kirchenbuechler, David; Flozak, Annette S; Gottardi, Cara J; Cuda, Carla M; Perlman, Harris; Jain, Manu; Kamp, David W; Budinger, G R Scott; Misharin, Alexander V
The European respiratory journal, 01/2020, Letnik: 55, Številka: 1Journal Article
Ontologically distinct populations of macrophages differentially contribute to organ fibrosis through unknown mechanisms.We applied lineage tracing, single-cell RNA sequencing and single-molecule fluorescence hybridisation to a spatially restricted model of asbestos-induced pulmonary fibrosis.We demonstrate that tissue-resident alveolar macrophages, tissue-resident peribronchial and perivascular interstitial macrophages, and monocyte-derived alveolar macrophages are present in the fibrotic niche. Deletion of monocyte-derived alveolar macrophages but not tissue-resident alveolar macrophages ameliorated asbestos-induced lung fibrosis. Monocyte-derived alveolar macrophages were specifically localised to fibrotic regions in the proximity of fibroblasts where they expressed molecules known to drive fibroblast proliferation, including platelet-derived growth factor subunit A. Using single-cell RNA sequencing and spatial transcriptomics in both humans and mice, we identified macrophage colony-stimulating factor receptor (M-CSFR) signalling as one of the novel druggable targets controlling self-maintenance and persistence of these pathogenic monocyte-derived alveolar macrophages. Pharmacological blockade of M-CSFR signalling led to the disappearance of monocyte-derived alveolar macrophages and ameliorated fibrosis.Our findings suggest that inhibition of M-CSFR signalling during fibrosis disrupts an essential fibrotic niche that includes monocyte-derived alveolar macrophages and fibroblasts during asbestos-induced fibrosis.
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