ArticleAmerican journal of respiratory cell and molecular biology2015
Induction of STAT3-Dependent CXCL5 Expression and Neutrophil Recruitment by Oncostatin-M during Pneumonia.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Plasma proteomic and machine learning models for differentiating idiopathic pulmonary fibrosis and connective tissue disease-associated interstitial lung disease: findings from a prospective cohort.Respiratory research · 2026Article
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Integrative blood profiling uncovers inflammatory network signatures in high-altitude pulmonary edema.Bioscience reports · 2025Article
- Article
- Hepatocyte iron suppresses liver fibrosis via fibrolytic neutrophil recruitment in cholestasis.JHEP reports : innovation in hepatology · 2025Article
- Transcriptomic responses of lung mesenchymal cells during pneumonia.JCI insight · 2025Article
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- TET2-STAT3-CXCL5 nexus promotes neutrophil lipid transfer to fuel lung adeno-to-squamous transition.The Journal of experimental medicine · 2024Article
- Constructing models for Crohn's disease diagnosis and prediction of infliximab non-response based on angiogenesis-related genes.Frontiers in immunology · 2024Article
- Epithelial STAT3: A New Twist in Inducible Antimicrobial Resistance.American journal of respiratory cell and molecular biology · 2023Article
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Analysis of Correlation Between Serum Oncostatin-M and Disease Severity and Mortality in Hospitalized Patients with Community-Acquired Pneumonia.Journal of inflammation research · 2023Article
- Epithelial LIF signaling limits apoptosis and lung injury during bacterial pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Integrative analysis reveals mouse strain-dependent responses to acute ozone exposure associated with airway macrophage transcriptional activity.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Identification of RAGE and OSM as New Prognosis Biomarkers of Severe Pneumonia.Canadian respiratory journal · 2022Article
- Neutrophil-Derived Oncostatin M Triggers Diverse Signaling Pathways during Pneumonia.Infection and immunity · 2021Article
- MicroRNA-4485 ameliorates severe influenza pneumonia via inhibition of the STAT3/PI3K/AKT signaling pathway.Oncology letters · 2020Article
- Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages.Journal of leukocyte biology · 2020Article
- Pneumonia recovery reprograms the alveolar macrophage pool.JCI insight · 2020Article
- Oncostatin M in the Regulation of Connective Tissue Cells and Macrophages in Pulmonary Disease.Biomedicines · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute bacterial pneumonia is a significant public health concern worldwide. Understanding the signals coordinating lung innate immunity may foster the development of therapeutics that limit tissue damage and promote host defense. We have previously shown that lung messenger RNA expression of the IL-6 family cytokine oncostatin-M (OSM) is significantly elevated in response to bacterial stimuli. However, its physiological significance during pneumonia is unknown. Here we demonstrate that OSM is rapidly increased in the airspaces of mice after pulmonary infection with Escherichia coli. Neutralization of OSM caused a substantial decrease in airspace neutrophils and macrophages. OSM blockade also caused a marked reduction in lung chemokine (C-X-C motif) ligand (CXCL) 5 expression, whereas other closely related neutrophil chemokines, CXCL1 and CXCL2, were unaffected. Intratracheal administration of recombinant OSM was sufficient to recapitulate the effect on CXCL5 induction, associated with robust activation of the signal transducer and activator of transcription 3 (STAT3) transcription factor. Cell sorting revealed that OSM effects were specific to lung epithelial cells, including a positive feedback loop in which OSM may facilitate expression of its own receptor. Finally, in vitro studies demonstrated that STAT3 was required for maximal OSM-induced CXCL5 expression. These studies demonstrate a novel role for OSM during pneumonia as an important signal to epithelial cells for chemokine induction mediating neutrophil recruitment.
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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.