ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Loss of CCR2 signaling alters leukocyte recruitment and exacerbates γ-herpesvirus-induced pneumonitis and fibrosis following bone marrow transplantation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Blood fibrocytes are associated with severity and prognosis in COVID-19 pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2021Trial
- Chemokine Receptor 2-targeted Molecular Imaging in Pulmonary Fibrosis. A Clinical Trial.American journal of respiratory and critical care medicine · 2021Trial
- Targeted lungScience advances · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- CD103+ dendritic cell-fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis.JCI insight · 2025Article
- Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures.Respiratory research · 2024Article
- Mesenchymal stem cell application in pulmonary disease treatment with emphasis on their interaction with lung-resident immune cells.Frontiers in immunology · 2024Review
- Microbiosis in lung allotransplantation and xenotransplantation: State of the art and future perspective.Health care science · 2022Review
- ZC3H4 regulates infiltrating monocytes, attenuating pulmonary fibrosis through IL-10.Respiratory research · 2022Article
- Mesenchymal stem cells alleviate idiopathic pneumonia syndrome by modulating T cell function through CCR2-CCL2 axis.Stem cell research & therapy · 2021Article
- Stem cell transplantation uncovers TDO-AHR regulation of lung dendritic cells in herpesvirus-induced pathology.JCI insight · 2021Article
- IRAK-M Regulates Monocyte Trafficking to the Lungs in Response to Bleomycin Challenge.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Diverse Injury Pathways Induce Alveolar Epithelial Cell CCL2/12, Which Promotes Lung Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- IL-17A Contributes to Lung Fibrosis in a Model of Chronic Pulmonary Graft-versus-host Disease.Transplantation · 2019Article
- A pathologic two-way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity.Clinical & translational immunology · 2019Review
- Lung Dysbiosis, Inflammation, and Injury in Hematopoietic Cell Transplantation.American journal of respiratory and critical care medicine · 2018Article
- Fibrocytes are increased in lung and peripheral blood of patients with idiopathic pulmonary fibrosis.Respiratory research · 2018Article
- Bone marrow transplant-induced alterations in Notch signaling promote pathologic Th17 responses to γ-herpesvirus infection.Mucosal immunology · 2018Article
- Fibrocyte migration, differentiation and apoptosis during the corneal wound healing response to injury.Experimental eye research · 2018Article
- Location or origin? What is critical for macrophage propagation of lung fibrosis?The European respiratory journal · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
CCR2-expressing leukocytes are required for the progression of fibrosis in models of induced lung injury as well as models of bone marrow transplant (BMT)-related idiopathic pneumonia syndrome. Infection with murid γ-herpesvirus-68 (γHV-68) results in severe pneumonitis and pulmonary fibrosis following syngeneic BMT; however, the roles that various proinflammatory leukocyte populations play in this process remain unclear. Deletion of CCR2 in both non-BMT and BMT mice increased early lytic viral replication and resulted in a reduction in the numbers of lung-infiltrating GR1+,F4/80+ and CXCR1+ cells, while maintaining robust neutrophil infiltration. Similarly, in γHV-68-infected CCR2(-/-) BMT mice, recruitment of monocytes and lymphocytes were reduced whereas neutrophil recruitment was increased compared with wild-type (WT) BMT mice. Interestingly, levels of profibrotic IL-17 were increased in infected CCR2 BMT mice compared with WT BMT. Furthermore, an increase in lung-associated collagen was detected even though there was an overall decrease in the number of profibrotic CCR2+ fibrocytes detected in the lungs of CCR2(-/-) BMT mice. These data indicate that, contrary to most models of fibrosis, deletion of CCR2 offers no protection from γ-herpesvirus-induced pneumonitis and fibrosis, and, indeed, CCR2+ cells play a suppressive role during the development of pulmonary fibrosis following γ-herpesvirus infection post-BMT by limiting IL-7 and collagen production.
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