ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Implicating exudate macrophages and Ly-6C(high) monocytes in CCR2-dependent lung fibrosis following gene-targeted alveolar injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- The Role of Monocytes in the Natural History of Idiopathic Pulmonary Fibrosis: A Systematic Literature Review.International journal of molecular sciences · 2025Pooled it
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- GDF15 participates in epithelial cell senescence in radiation-induced lung injury through the ERK1/2-p16 signaling pathway.PloS one · 2026Article
- Mendelian Randomization Reveals Genetic Associations Between Immune Traits and Urethral Stricture.Mediators of inflammation · 2026Article
- Radiation-induced Lung Injury (RILI) in Non-human Primates (NHPs) Induces Cellular Senescence and Upregulation of Tyrosine Kinase Fgr, which is Detectable in Bronchoalveolar Lavage.Radiation research · 2025Article
- Epithelial damage and ageing: the perfect storm.Thorax · 2025Review
- YAP/TAZ are crucial regulators of macrophage-mediated pulmonary inflammation and fibrosis after bleomycin-induced injury.The European respiratory journal · 2025Article
- Human umbilical cord mesenchymal stem cell-derived microvesicles alleviate pulmonary fibrosis by inhibiting monocyte‒macrophage migration through ERK1/2 signaling-mediated suppression of CCL2 expression.Stem cell research & therapy · 2025Article
- The role of oxidative stress-related genes in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Human hypofunctional NCF1 variants promote pulmonary fibrosis in the bleomycin-induced mouse model and patients with systemic sclerosis via expansion of SPP1Annals of the rheumatic diseases · 2025Article
- The Intersection between Immune System and Idiopathic Pulmonary Fibrosis-A Concise Review.Fibrosis (Hong Kong, China) · 2025Article
- CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.Cell & bioscience · 2024Article
- Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures.Respiratory research · 2024Article
- Mammalian Target of Rapamycin Complex 1 Activation in Macrophages Contributes to Persistent Lung Inflammation following Respiratory Tract Viral Infection.The American journal of pathology · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- Regulation of epithelial transitional states in murine and human pulmonary fibrosis.The Journal of clinical investigation · 2023Article
- Identification of monocyte-associated pathways participated in the pathogenesis of pulmonary arterial hypertension based on omics-data.Pulmonary circulation · 2023Article
- L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2022Article
- Deciphering the Effects of 2D Black Phosphorus on Disrupted Hematopoiesis and Pulmonary Immune Homeostasis Using a Developed Flow Cytometry Method.Environmental science & technology · 2022Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The alveolar epithelium is characteristically abnormal in fibrotic lung disease, and we recently established a direct link between injury to the type II alveolar epithelial cell (AEC) and the accumulation of interstitial collagen. The mechanisms by which damage to the epithelium induces lung scarring remain poorly understood. It is particularly controversial whether an insult to the type II AEC initiates an inflammatory response that is required for the development of fibrosis. To explore whether local inflammation occurs following a targeted epithelial insult and contributes to lung fibrosis, we administered diphtheria toxin to transgenic mice with type II AEC-restricted expression of the diphtheria toxin receptor. We used immunophenotyping techniques and diphtheria toxin receptor-expressing, chemokine receptor-2-deficient (CCR2(-/-)) mice to determine the participation of lung leukocyte subsets in pulmonary fibrogenesis. Our results demonstrate that targeted type II AEC injury induces an inflammatory response that is enriched for CD11b(+) nonresident exudate macrophages (ExM) and their precursors, Ly-6C(high) monocytes. CCR2 deficiency abrogates the accumulation of both cell populations and protects mice from fibrosis, weight loss, and death. Further analyses revealed that the ExM are alternatively activated and that ExM and Ly-6C(high) monocytes express mRNA for IL-13, TGF-β, and the collagen genes, COL1A1 and COLIIIA1. Furthermore, the accumulated ExM and Ly-6C(high) monocytes contain intracellular collagen, as detected by immunostaining. Together, these results implicate CCR2 and the accumulation of ExM and Ly-6C(high) monocytes as critical determinants of pulmonary fibrosis induced by selective type II AEC injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.