ArticleAmerican journal of respiratory cell and molecular biology2019
IL-9 Blockade Suppresses Silica-induced Lung Inflammation and Fibrosis in Mice.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- A Review of CXCL1 in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2021Pooled it
- Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Alveolar-Basal Intermediates Drive Pulmonary Fibrosis via Coordination of a Pro-Fibrotic Signaling Niche in Silicosis.bioRxiv : the preprint server for biology · 2026Article
- Activation of TSLP-IL-9 Axis Hinders the Antifibrotic Effect of ST2 Deficiency in Pulmonary Fibrosis.International journal of molecular sciences · 2025Article
- A Simple Ratio in a Complex Disease: Exploring the Neutrophil-to-Lymphocyte Ratio in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Sustained Release of Antifibrotic Nintedanib from Polymer Microparticles Reduces Dosing Frequency While Reducing Inflammation in Murine Idiopathic Pulmonary Fibrosis.Annals of biomedical engineering · 2025Article
- CD4Frontiers in immunology · 2025Review
- Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.Frontiers in medicine · 2025Review
- Predicting biomarkers of progressive pulmonary fibrosis: morphological, cytokine profile, and clinical portrait.Frontiers in immunology · 2025Article
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
- Short- and long-term pathologic responses to quartz are induced by nearly free silanols formed during crystal fracturing.Particle and fibre toxicology · 2024Article
- Interleukin-9 promotes EMT-mediated PMArchives of toxicology · 2024Article
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- The Role of Immune Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2023Review
- Review
- IL-9 aggravates SARS-CoV-2 infection and exacerbates associated airway inflammation.Nature communications · 2023Article
- Upregulated Expression of the IL-9 Receptor on TRAF3-Deficient B Lymphocytes Confers Ig Isotype Switching Responsiveness to IL-9 in the Presence of Antigen Receptor Engagement and IL-4.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Effects of Green Tea Polyphenol Epigallocatechin-3-Gallate on Markers of Inflammation and Fibrosis in a Rat Model of Pulmonary Silicosis.International journal of molecular sciences · 2023Article
- Thrombocyte-derived Dickkopf1 promotes macrophage polarization in the Bleomycin-induced lung injury model.Frontiers in immunology · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recapitulative animal models of idiopathic pulmonary fibrosis (IPF) and related diseases are lacking, which inhibits our ability to fully clarify the pathogenesis of these diseases. Although lung fibrosis in mouse models is often induced by bleomycin, silica-induced lung fibrosis is more sustainable and more progressive. Therefore, in this study, we sought to elucidate the mediator(s) responsible for the pathogenesis of lung fibrosis, through the use of a mouse model of silica-induced lung fibrosis. With a single nasal administration of 16 mg of silica, lung inflammation (assessed by elevated cellular components in the BAL fluids [BALFs]) and lung fibrosis (assessed by lung histology and lung hydroxyproline levels) were induced and sustained for as long as 24 weeks. Of the mediators measured in the BALFs, IL-9 was characteristically elevated gradually, and peaked at 24 weeks after silica administration. Treatment of silica-challenged mice with anti-IL-9-neutralizing antibody inhibited lung fibrosis, as assessed by lung hydroxyproline level, and suppressed the levels of major mediators, including IL-1β, IL-6, IL-12, CCL2, CXCL1, and TNF-α in BALFs. Moreover, human lung specimens from patients with IPF have shown high expression of IL-9 in alveolar macrophages, CD4-positive cells, and receptors for IL-9 in airway epithelial cells. Collectively, these data suggest that IL-9 plays an important role in the pathogenesis of lung fibrosis in diseases such as IPF.
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