ArticleJCI insight2020
FPR-1 is an important regulator of neutrophil recruitment and a tissue-specific driver of pulmonary fibrosis.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
61 citing papers in PubMed, 98 citations in OpenAlex.
- N-Formyl Methionine Peptide-Mediated Neutrophil Activation in Systemic Sclerosis.Frontiers in immunology · 2021Trial
- Δ9-Tetrahydrocannabinol exposure shifts eosinophil and macrophage transcriptional programs toward an anti-inflammatory phenotype in helminth infection.Journal of leukocyte biology · 2026Article
- Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.Expert reviews in molecular medicine · 2026Review
- Heterozygous variants in DOCK2 leading to susceptibility to viral illnesses.The Journal of allergy and clinical immunology · 2026Article
- Myeloperoxidase promotes fibrosis by inhibiting cathepsin K to bias the lung toward ECM accumulation.bioRxiv : the preprint server for biology · 2026Article
- Galectin-9Aging cell · 2026Article
- Article
- Inhibition of MAPK p38α overcomes the cancer immunosurveillance defect caused by FPR1 loss-of-function mutation.Cell reports. Medicine · 2026Article
- Airway injury induces alveolar epithelial responses mediated by macrophages.Cell reports · 2026Article
- Quantitative proteomics and phosphoproteomics reveal glucocorticoid stimulation of TLR and Rho GTPase signaling in neutrophil-like cells.Genome biology · 2026Article
- The role of immune cell crosstalk and signaling pathways in the pathogenesis of pulmonary fibrosis.Molecular biology reports · 2026Review
- How the Fibrotic Lung Microenvironment Regulates Stem Cell Behavior: Immune Cues, Extracellular Matrix Remodeling, and Therapeutic Implications.Analytical cellular pathology (Amsterdam) · 2026Review
- GPCRs as key regulators in wound healing.Frontiers in cell and developmental biology · 2026Review
- Systemic neutrophil activation and N-formyl methionine-formyl peptide receptor-1 signaling define inflammatory endotypes in rheumatoid arthritis-associated lung involvement.Journal of internal medicine · 2025Article
- Mesenchymal stromal cell extracellular vesicles reduceAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- Formyl peptide receptor 1 and its antagonist T0080 in atherosclerosis.Cell death and differentiation · 2025Article
- Pericytes change function depending on glioblastoma vicinity: emphasis on immune regulation.Molecular oncology · 2025Article
- Temporal dichotomy of neutrophil function in acute liver injury and repair.JHEP reports : innovation in hepatology · 2025Article
- Let-7b-5p loaded Mesenchymal Stromal Cell Extracellular Vesicles reducebioRxiv : the preprint server for biology · 2025Article
- Article
1 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
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Neutrophils are the most abundant inflammatory cells at the earliest stages of wound healing and play important roles in wound repair and fibrosis. Formyl peptide receptor 1 (FPR-1) is abundantly expressed on neutrophils and has been shown to regulate their function, yet the importance of FPR-1 in fibrosis remains ill defined. FPR-1-deficient (fpr1-/-) mice were protected from bleomycin-induced pulmonary fibrosis but developed renal and hepatic fibrosis normally. Mechanistically, we observed a failure to effectively recruit neutrophils to the lungs of fpr1-/- mice, whereas neutrophil recruitment was unaffected in the liver and kidney. Using an adoptive transfer model we demonstrated that the defect in neutrophil recruitment to the lung was intrinsic to the fpr1-/- neutrophils, as C57BL/6 neutrophils were recruited normally to the damaged lung in fpr1-/- mice. Finally, C57BL/6 mice in which neutrophils had been depleted were protected from pulmonary fibrosis. In conclusion, FPR-1 and FPR-1 ligands are required for effective neutrophil recruitment to the damaged lung. Failure to recruit neutrophils or depletion of neutrophils protects from pulmonary 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.