ArticleThe American journal of pathology2005
Role of Eotaxin-1 (CCL11) and CC chemokine receptor 3 (CCR3) in bleomycin-induced lung injury and fibrosis.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- The bleomycin animal model: a useful tool to investigate treatment options for idiopathic pulmonary fibrosis?The international journal of biochemistry & cell biology · 2008Pooled it
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- Bronchoalveolar lavage cell differential count is associated with survival and radiological UIP pattern in familial pulmonary fibrosis.BMC pulmonary medicine · 2026Article
- Bone marrow CCR3 dictates eosinophil lineage commitment of CD34⁺ progenitors to orchestrate allergic rhinitis: A composite study.PloS one · 2026Article
- Persistent neurological and behavioral alterations after SARS-CoV-2 infection in an optimized K18-hACE2 mouse model.Frontiers in microbiology · 2026Article
- Fibroblast-centered mechanisms of chronic inflammation and airway remodeling in allergic bronchopulmonary aspergillosis.Frontiers in allergy · 2026Review
- Proteomic analysis identifies novel molecular signatures and immune-metabolic pathways in rheumatoid arthritis-associated interstitial lung disease.Biomedical reports · 2025Article
- Batch correcting single-cell spatial transcriptomics count data with Crescendo improves visualization and detection of spatial gene patterns.Genome biology · 2025Article
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- The Association of Blood Eosinophils and Neutrophils Expressing Eosinophilic Surface Markers with the Severity and Outcome of COVID-19.Microorganisms · 2024Article
- Eosinophilic inflammation: a key player in COPD pathogenesis and progression.Annals of medicine · 2024Review
- Deregulated immune cell recruitment orchestrated by c-MET impairs pulmonary inflammation and fibrosis.Respiratory research · 2024Article
- CC Chemokine Family Members' Modulation as a Novel Approach for Treating Central Nervous System and Peripheral Nervous System Injury-A Review of Clinical and Experimental Findings.International journal of molecular sciences · 2024Review
- Disease Course, Treatments, and Outcomes of Children With Systemic Juvenile Idiopathic Arthritis-Associated Lung Disease.Arthritis care & research · 2024Article
- The study of the role of purified anti-mouse CD193 (CCR3) antibody in allergic rhinitis mouse animal models.Scientific reports · 2024Article
- A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence.Immunity & ageing : I & A · 2023Article
- C-C motif chemokine CCL11 is a novel regulator and a potential therapeutic target in non-alcoholic fatty liver disease.JHEP reports : innovation in hepatology · 2023Article
- Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain.Molecules (Basel, Switzerland) · 2023Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Eotaxin-1/CCL11 and its receptor CCR3 are involved in recruitment of eosinophils to diverse tissues, but their role in eosinophil recruitment in pulmonary fibrosis is unclear. The present study examined the pulmonary expression of CCL11 and CCR3 during bleomycin (blm)-induced lung injury and determined their importance in the recruitment of inflammatory cells and the development of lung fibrosis. In mice, blm induced a marked pulmonary expression of CCL11 and CCR3. Immunostaining for CCR3 revealed that this receptor was not only expressed by eosinophils but also by neutrophils. CCL11-deficient (CCL11(-/-)) mice developed significantly reduced pulmonary fibrosis. Expression of profibrotic cytokines such as transforming growth factor-beta1 was diminished in the absence of CCL11. Furthermore, increased lung expression of CCL11 significantly enhanced blm-induced lung fibrosis and production of profibrotic cytokines. These effects were also associated with an increase of eosinophil and neutrophil pulmonary infiltration. In contrast, mice treated with neutralizing CCR3 antibodies developed significantly reduced pulmonary fibrosis, eosinophilia, neutrophilia, and expression of profibrotic cytokines. Together, these data suggest that CCL11 and CCR3 are important in the pulmonary recruitment of granulocytes and play significant pathogenic roles in blm-induced lung fibrosis.
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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.