Profibrotic properties of C1q interstitial macrophages in silica-induced pulmonary fibrosis in mice.

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ID: 275039
2022
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Ranked #21 of 66 articles by views in Biochemical and biophysical research communications

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Abstract
Pulmonary fibrosis (PF) is a progressive fibrotic disease with poor prognosis and suboptimal therapeutic options. Although macrophages have been implicated in PF, the role of macrophage subsets, particularly interstitial macrophages (IMs), remains unknown. We performed a time-series single-cell RNA sequencing analysis of the silica-induced mouse PF model. Among the macrophage subsets in fibrotic lungs, Lyve1 MHC II IMs increased with fibrosis, and highly expressed profibrotic genes. Additionally, we identified C1q as an IM-specific marker. Experiments with C1q-diphtheria toxin receptor-GFP knock-in (C1qKI) mice revealed that IMs are distributed around fibrotic nodules. Depletion of C1q IMs in C1qKI mice decreased activated fibroblasts and epithelial cells; however, bodyweight loss and neutrophil infiltration were exacerbated in silica-induced PF. Collectively, these results suggest that IMs have profibrotic and anti-inflammatory properties and that the selective inhibition of the profibrotic function of IMs without compromising their anti-inflammatory effects is a potential novel therapeutic strategy for PF.
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ogawa2022profibroticbiochemical Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Tatsuro Ogawa, Shigeyuki Shichino, Satoshi Ueha, Kana Bando, Kouji Matsushima
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Journal Biochemical and biophysical research communications
Year 2022
DOI
S0006-291X(22)00226-1
URL
Keywords
macrophage single-cell rna sequencing pulmonary fibrosis fibroblast ccr2

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