ArticleAmerican journal of respiratory cell and molecular biology2014
Proteinase-activated receptor-1, CCL2, and CCL7 regulate acute neutrophilic lung inflammation.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 92 citations in OpenAlex.
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- Systemic inflammatory response drives post-cardiac arrest multi-organ injury via IL-17 signaling in murine and porcine models.Frontiers in immunology · 2026Article
- Single-cell RNA sequencing identifies ZBP1-dependent mechanisms in OSCC progression.Cell death & disease · 2025Article
- Obtusifolin mitigates acute lung injury and improves cardio-pulmonary functions in acute lung injury model by modulating oxidative stress and NF-κB signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Single-Cell Transcriptomic Profiling Reveals a Distinct Monocyte MIF/ANXA1 Signature Associated With Poor Responsiveness to ICS.Allergy, asthma & immunology research · 2025Article
- Epigenetic Regulation of Neutrophils in ARDS.Cells · 2025Review
- Role of Tumor Necrosis Factor in Tuberculosis.Biomolecules · 2025Review
- CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis.iScience · 2025Article
- Tissue inflammation induced by constitutively active STING is mediated by enhanced TNF signaling.eLife · 2025Article
- Immunomodulatory role of the stem cell circadian clock in muscle repair.Science advances · 2025Article
- C-C Motif Ligand 7 and C-C Motif Chemokine Receptor 3 Dysregulation in Patients With Scrub Typhus and Association With Mortality.The Journal of infectious diseases · 2025Article
- Protease-activated receptor 1 in the pathogenesis of cystic fibrosis.BMJ open respiratory research · 2025Article
- Calcitriol Administration Attenuates Acute Lung Injury by Improving Angiopoietin/Tie2 Dysregulation and Alveolar-Capillary Barrier Integrity in a Mouse Model of Ovariectomy Complicated With Sepsis.Mediators of inflammation · 2025Article
- Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling.The Journal of clinical investigation · 2024Article
- The link between neutrophils, NETs, and NLRP3 inflammasomes: The dual effect of CD177 and its therapeutic potential in acute respiratory distress syndrome/acute lung injury.Biomolecules & biomedicine · 2024Article
- Pharmacological profile of dicaffeoylquinic acids and their role in the treatment of respiratory diseases.Frontiers in pharmacology · 2024Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
PAR1 plays a central role in mediating the interplay between coagulation and inflammation, but its role in regulating acute neutrophilic inflammation is unknown. We report that antagonism of PAR1 was highly effective at reducing acute neutrophil accumulation in a mouse model of LPS-induced lung inflammation. PAR1 antagonism also reduced alveolar-capillary barrier disruption in these mice. This protection was associated with a reduction in the expression of the chemokines, CCL2 and CCL7, but not the proinflammatory cytokines, TNF and IL-6, or the classic neutrophil chemoattractants, CXCL1 and CXCL2. Antibody neutralization of CCL2 and CCL7 significantly reduced LPS-induced total leukocyte and neutrophil accumulation, recovered from the bronchoalveolar lavage fluid of challenged mice. Immunohistochemical analysis revealed that CCL2 predominantly localized to alveolar macrophages and pulmonary epithelial cells, whereas CCL7 was restricted to the pulmonary epithelium. In keeping with these observations, the intranasal administration of recombinant CCL2 (rCCL2) and rCCL7 led to the accumulation of neutrophils within the lung airspaces of naive mice in the absence of any underlying inflammation. Flow cytometry analysis further demonstrated an increase in Ly6G(hi) neutrophils expressing the chemokine receptors, CCR1 and CCR2, isolated from mouse lungs compared with circulating neutrophils. Conversely, the expression of CXCR2 decreased on neutrophils isolated from the lung compared with circulating neutrophils. Furthermore, this switch in chemokine receptor expression was accentuated after acute LPS-induced lung inflammation. Collectively, these findings reveal a novel role for PAR1 and the chemokines, CCL2 and CCL7, during the early events of acute neutrophilic inflammation.
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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.