ArticleJournal of translational medicine2018
Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- The multistep progression of areca nut-induced oral cancer: a mechanistic roadmap from pathogenesis to precision therapy.Life medicine · 2026Review
- Spatial Transcriptomic and Metabolomic Landscapes of Oral Submucous Fibrosis-Derived Oral Squamous Cell Carcinoma and its Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Natural Killer Cells as a Further Insight into the Course of Chronic Obstructive Pulmonary Disease.Biomedicines · 2024Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- Role and mechanism of benzo[a]pyrene in the transformation of chronic obstructive pulmonary disease into lung adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Macrophage Polarization: An Important Candidate Regulator for Lung Diseases.Molecules (Basel, Switzerland) · 2023Review
- Analyses of Factors Associated with Acute Exacerbations of Chronic Obstructive Pulmonary Disease: A Review.International journal of chronic obstructive pulmonary disease · 2023Review
- Article
- Single-Cell Transcriptome Analysis Reveals Inter-Tumor Heterogeneity in Bilateral Papillary Thyroid Carcinoma.Frontiers in immunology · 2022Article
- Small extracellular vesicles derived from interferon-γ pre-conditioned mesenchymal stromal cells effectively treat liver fibrosis.NPJ Regenerative medicine · 2021Article
- Regulation of Inflammation and Oxidative Stress by Formyl Peptide Receptors in Cardiovascular Disease Progression.Life (Basel, Switzerland) · 2021Review
- Acute cigarette smoke-induced eQTL affects formyl peptide receptor expression and lung function.Respirology (Carlton, Vic.) · 2021Article
- NK Cells in the Pathogenesis of Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2021Review
- Formyl peptide receptors in the mucosal immune system.Experimental & molecular medicine · 2020Review
- Novel formyl peptide receptor (FPR) agonists with pyridinone and pyrimidindione scaffolds that are potentially useful for the treatment of rheumatoid arthritis.Bioorganic chemistry · 2020Article
- Identification of differentially expressed genes and signaling pathways in chronic obstructive pulmonary disease via bioinformatic analysis.FEBS open bio · 2019Article
- Chemotactic Ligands that Activate G-Protein-Coupled Formylpeptide Receptors.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundControversy exists in previous studies on macrophage M1/M2 polarization in chronic obstructive pulmonary disease (COPD). We hypothesized that formyl peptide receptor (FPR), a marker of efferocytosis and mediator of M1/M2 polarization, may be involved in the development of COPD.
methodsWe examined FPR 1/2/3 expressions of blood M1/M2a monocyte, neutrophil, natural killer (NK) cell, NK T cell, T helper (Th) cell, and T cytotoxic (Tc) cell by flowcytometry method in 40 patients with cigarette smoking-related COPD and 16 healthy non-smokers. Serum levels of five FPR ligands were measured by ELISA method.
resultsThe COPD patients had lower M2a percentage and higher percentages of NK, NK T, Th, and Tc cells than the healthy non-smokers. FPR2 expressions on Th/Tc cells, FPR3 expressions of M1, M2a, NK, NK T, Th, and Tc cells, and serum annexin A1 (an endogenous FPR2 ligand) levels were all decreased in the COPD patients as compared with that in the healthy non-smokers. FPR1 expression on neutrophil was increased in the COPD patient with a high MMRC dyspnea scale, while FPR2 expression on neutrophil and annexin A1 were both decreased in the COPD patients with a history of frequent moderate exacerbation (≥ 2 events in the past 1 year). In 10 COPD patients whose blood samples were collected again after 1-year treatment, M2a percentage, FPR3 expressions of M1/NK/Th cells, FPR2 expression on Th cell, and FPR1 expression on neutrophil were all reversed to normal, in parallel with partial improvement in small airway dysfunction.
conclusionsOur findings provide evidence for defective FPR2/3 and annexin A1 expressions that, associated with decreased M2a polarization, might be involved in the development of cigarette smoking induced persistent airflow limitation in COPD.
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