ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
Organic dust induces inflammatory gene expression in lung epithelial cells via ROS-dependent STAT-3 activation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- A systematic review of environmentally persistent free radical (EPFR) formation, characteristics, and health effects: are there sufficient data for risk assessment?Journal of toxicology and environmental health. Part B, Critical reviews · 2026Pooled it
- Aryl hydrocarbon receptor (AhR) regulates organic dust and organic dust-associated bacterial extracellular vesicles-induced airway inflammation via ROS-dependent NFκB and STAT3 activation.Respiratory research · 2026Article
- Genetic Susceptibility to Impaired Lung Function in Underground Coal Miners from Kazakhstan.Genes · 2026Article
- Redox-sensitive GPCR signaling drives Gq-dependent CaAmerican journal of physiology. Cell physiology · 2026Article
- Endoplasmic Reticulum Stress and Unfolded Protein Response Sensor ERN1 Regulates Organic Dust Induction of Lung Inflammation.FASEB bioAdvances · 2025Article
- Epac1 Inhibits Orbital Fibroblast Activation to Ameliorate Thyroid-Associated Orbitopathy-Like Features Through the JAK/STAT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
- Multiphase Radical Chemical Processes Induced by Air Pollutants and the Associated Health Effects.Environment & health (Washington, D.C.) · 2025Review
- Particulate Matter-Induced Emerging Health Effects Associated with Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure.Journal of immunotoxicology · 2023Article
- Purification and characterization of a serine protease from organic dust and elucidation of its inductive effects on lung inflammatory mediators.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- New Therapeutic Horizon of Graves' Hyperthyroidism: Treatment Regimens Based on Immunology and Ingredients From Traditional Chinese Medicine.Frontiers in pharmacology · 2022Review
- Bacterial extracellular vesicles isolated from organic dust induce neutrophilic inflammation in the lung.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Amphiregulin modulates murine lung recovery and fibroblast function following exposure to agriculture organic dust.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Research on the Potential Mechanism of Gypenosides on Treating Thyroid-Associated Ophthalmopathy Based on Network Pharmacology.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
- Erratum issuedCORRIGENDUM.2019
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to dust in agricultural and animal environments, known as organic dust, is associated with the development of respiratory symptoms and respiratory diseases. Inflammation is a key feature of lung pathologies associated with organic dust exposure, and exposure to organic dust induces the expression of several immune and inflammatory mediators. However, information on transcription factors and cellular and molecular mechanisms controlling the production of immune and inflammatory mediators induced by organic dust is limited. In this study, we have identified STAT-3 as an important transcription factor controlling the induction of expression of immune and inflammatory mediators by poultry dust extracts in airway epithelial cells and in mouse lungs and delineated the cellular pathway for STAT-3 activation. Poultry dust extract activated STAT-3 phosphorylation in Beas2B and normal human bronchial epithelial cells and in mouse lungs. Chemical inhibition and siRNA knockdown of STAT-3 suppressed induction of immune and inflammatory mediator expression. Antioxidants suppressed the increase of STAT-3 phosphorylation induced by poultry dust extract indicating that oxidative stress [elevated reactive oxygen species (ROS) levels] is important for the activation. Chemical inhibition and siRNA knockdown experiments demonstrated that STAT-3 activation is dependent on the activation of nonreceptor tyrosine-protein kinase 2 (TYK2) and epidermal growth factor receptor (EGFR) tyrosine kinases. Our studies show that poultry dust extract controls the induction of immune and inflammatory mediator expression via a cellular pathway involving oxidative stress-mediated STAT-3 activation by TYK2 and EGFR tyrosine kinases.
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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.