ArticleThe Journal of allergy and clinical immunology2017
Neutrophils are a major source of the epithelial barrier disrupting cytokine oncostatin M in patients with mucosal airways disease.
Article in The Journal of allergy and clinical immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- Roles of PI3K pan-inhibitors and PI3K-δ inhibitors in allergic lung inflammation: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- TLR7 alters the maternal immune landscape during influenza A infection to increase maternal and fetal morbidity.Science advances · 2026Article
- A bibliometric analysis of trends and hotspots in Oncostatin M.Discover oncology · 2026Article
- Why, Immunologically, Housing-Related Fungi and Endotoxins (and Other Chronic Pro-Inflammatory Stressors) Risk Latent Tuberculosis Reactivation, Severe Asthma, and Translocating and Invasive Infections in Indigenous Communities in Canada.American journal of human biology : the official journal of the Human Biology Council · 2026Review
- Basophils activate oncostatin M receptor-expressing vagal sensory neurons.The Journal of allergy and clinical immunology · 2026Article
- Effects of type 3 and neutrophilic inflammation on type 2 chronic rhinosinusitis with nasal polyps.The Journal of allergy and clinical immunology · 2026Article
- Stigmasterol Decreases Oncostatin M Production Through Suppressing PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells.Biomedicines · 2026Article
- Neutrophil-derived oncostatin m contributes to endothelial cell dysfunction during Treponema denticola interaction.PloS one · 2026Article
- Progress in cellular mechanisms of chronic rhinosinusitis.Fundamental research · 2026Review
- Integrative blood profiling uncovers inflammatory network signatures in high-altitude pulmonary edema.Bioscience reports · 2025Article
- Neutrophil Heterogeneity in Airway Inflammatory Diseases.Inflammation · 2025Review
- Distinct Effects of Biological Treatments on Eosinophils and Neutrophils in Chronic Rhinosinusitis With Nasal Polyp Patients.Clinical and translational allergy · 2025Article
- Bacterial communities co-develop with respiratory immunity early in life, linking dysbiosis to systemic monocyte signature and wheezing.Science advances · 2025Article
- [Advances in the pathogenesis and treatment of neutrophils in chronic sinusitis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Review
- Bronchiectasis and sinonasal diseases: a narrative review.ERJ open research · 2025Review
- Differential Immune Cell Infiltration in Eosinophilic and Non-Eosinophilic CRS: Correlations With Clinical, Endoscopic, and Radiological Findings.International forum of allergy & rhinology · 2025Article
- Transcriptomic Profiling of the Immune Response in Orthotopic Pancreatic Tumours Exposed to Combined Boiling Histotripsy and Oncolytic Reovirus Treatment.Pharmaceutics · 2025Article
- Nonlinear association between neutrophil-to-lymphocyte ratio and asthma in children and adolescents in the United States: a cross-sectional study.Clinical and experimental pediatrics · 2025Article
- Mechanical force-induced oncostatin M secretion by Jun-positive neutrophils promotes craniofacial bone regeneration for midface hypoplasia treatment.Stem cell research & therapy · 2025Article
35 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
18 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundWe have previously shown that oncostatin M (OSM) levels are increased in nasal polyps (NPs) of patients with chronic rhinosinusitis (CRS), as well as in bronchoalveolar lavage fluid, after segmental allergen challenge in allergic asthmatic patients. We also showed in vitro that physiologic levels of OSM impair barrier function in differentiated airway epithelium.
objectiveWe sought to determine which hematopoietic or resident cell type or types were the source of the OSM expressed in patients with mucosal airways disease.
methodsParaffin-embedded NP sections were stained with fluorescence-labeled specific antibodies against OSM, GM-CSF, and hematopoietic cell-specific markers. Live cells were isolated from NPs and matched blood samples for flow cytometric analysis. Neutrophils were isolated from whole blood and cultured with the known OSM inducers GM-CSF and follistatin-like 1, and OSM levels were measured in the supernatants. Bronchial biopsy sections from control subjects, patients with moderate asthma, and patients with severe asthma were stained for OSM and neutrophil elastase.
resultsOSM staining was observed in NPs, showed colocalization with neutrophil elastase (n = 10), and did not colocalize with markers for eosinophils, macrophages, T cells, or B cells (n = 3-5). Flow cytometric analysis of NPs (n = 9) showed that 5.1% ± 2% of CD45
conclusionsNeutrophils are a major source of OSM-producing cells in patients with CRS and severe asthma.
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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.