ArticleThe American journal of pathology2008
A novel mechanism for CCR4 in the regulation of macrophage activation in bleomycin-induced pulmonary fibrosis.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 94 citations in OpenAlex.
- Blockade of IL-6 Trans signaling attenuates pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
- Review
- CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.Cell & bioscience · 2024Article
- CC Chemokines in Idiopathic Pulmonary Fibrosis: Pathogenic Role and Therapeutic Potential.Biomolecules · 2023Review
- Immune Mechanisms of Pulmonary Fibrosis with Bleomycin.International journal of molecular sciences · 2023Review
- Pleiotropic antifibrotic actions of aspirin-triggered resolvin D1 in the lungs.Frontiers in immunology · 2023Article
- Plasticity towards Rigidity: A Macrophage Conundrum in Pulmonary Fibrosis.International journal of molecular sciences · 2022Review
- Anti-Inflammatory Effects of Cicadidae Periostracum Extract and Oleic Acid through Inhibiting Inflammatory Chemokines Using PCR Arrays in LPS-Induced Lung inflammation In Vitro.Life (Basel, Switzerland) · 2022Article
- Emerging insights in sarcoidosis: moving forward through reverse translational research.American journal of physiology. Lung cellular and molecular physiology · 2022Review
- Cell Origin and iNOS Function Are Critical to Macrophage Activation Following Acute Lung Injury.Frontiers in pharmacology · 2021Article
- Targeting fibroblast CD248 attenuates CCL17-expressing macrophages and tissue fibrosis.Scientific reports · 2020Article
- Surfactant protein-D modulation of pulmonary macrophage phenotype is controlled byAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Modeling and multiscale characterization of the quantitative imaging based fibrosis index reveals pathophysiological, transcriptome and proteomic correlates of lung fibrosis induced by fractionated irradiation.International journal of cancer · 2019Article
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Expression of mutant Sftpc in murine alveolar epithelia drives spontaneous lung fibrosis.The Journal of clinical investigation · 2018Article
- Evolving notions on immune response in colorectal cancer and their implications for biomarker development.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Protective role of NKT cells and macrophage M2-driven phenotype in bleomycin-induced pulmonary fibrosis.Inflammopharmacology · 2018Article
- CCR2 contributes to the recruitment of monocytes and leads to kidney inflammation and fibrosis development.Inflammopharmacology · 2018Article
- TRAIL-Dependent Resolution of Pulmonary Fibrosis.Mediators of inflammation · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Macrophage polarization into M1 or M2 phenotypes dictates the nature, duration, and severity of an inflammatory response. The objective of this study was to examine the role of CC chemokine receptor 4 (CCR4) in macrophage polarization during pulmonary oxidative injury in wild-type [WT (CCR4(+/+))] and CCR4-deficient (CCR4(-/-)) mice. Intrapulmonary administration of bleomycin sulfate provoked lethal inflammatory and fibrotic responses in WT (CCR4(+/+)) mice, but such responses were absent in CCR4(-/-) mice. Transcript and protein analyses of alveolar and bone marrow-derived macrophages showed that cells isolated from CCR4(-/-) mice did not exhibit CCL17-dependent M1 activation in response to bleomycin. Instead, CCR4(-/-) macrophages showed an M2 phenotype characterized by significantly elevated expression of arginase 1 and FIZZ1 (found in inflammatory zone 1), particularly during the peak of pulmonary inflammation. Compared with WT (CCR4(+/+)) mice, CCR4(-/-) mice exhibited a significant increase in the expression of the nonsignaling CC chemokine scavenging receptor D6 in whole lung samples and isolated macrophages. Thus, these results demonstrate that CCL17-dependent activation of CCR4 in macrophages plays a central role in free radical-induced pulmonary injury and repair.
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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.