ArticleJournal of cellular and molecular medicine2014
Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Results from omic approaches in rat or mouse models exposed to inhaled crystalline silica: a systematic review.Particle and fibre toxicology · 2024Pooled it
- Evaluating the efficacy of prednisolone for silicosis with progressive massive fibrosis in Australia: an observational pilot study.Annals of occupational and environmental medicine · 2026Article
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis.Respiratory research · 2025Article
- CD4Frontiers in immunology · 2025Review
- Early diagnosis and survival outcomes in silicosis: a retrospective cohort study of 11,809 patients in Guangdong Province, China (1956-2020).Frontiers in public health · 2025Article
- Efficacy and safety of a whole lung lavage program for artificial stone silicosis.Journal of thoracic disease · 2024Article
- The role of inflammation in silicosis.Frontiers in pharmacology · 2024Review
- No causal association between pneumoconiosis and three inflammatory immune diseases: a Mendelian randomization study.Frontiers in public health · 2024Article
- Animal models of silicosis: fishing for new therapeutic targets and treatments.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- 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
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- SiOToxicology research · 2022Article
- MBL Binding with AhR Controls Th17 Immunity in Silicosis-Associated Lung Inflammation and Fibrosis.Journal of inflammation research · 2022Article
- Herbal compounds in the treatment of pulmonary silicosis.Physiological research · 2021Review
- Extracellular Heat Shock Proteins as Therapeutic Targets and Biomarkers in Fibrosing Interstitial Lung Diseases.International journal of molecular sciences · 2021Review
- New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis.International journal of molecular sciences · 2021Review
- Lipopolysaccharides promote pulmonary fibrosis in silicosis through the aggravation of apoptosis and inflammation in alveolar macrophages.Open life sciences · 2020Article
- Role of Nephronectin in Pathophysiology of Silicosis.International journal of molecular sciences · 2019Review
- Dihydrotanshinone I Alleviates Crystalline Silica-Induced Pulmonary Inflammation by Regulation of the Th Immune Response and Inhibition of STAT1/STAT3.Mediators of inflammation · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is an occupational lung disease caused by the inhalation of silica dust and characterized by lung inflammation and fibrosis. Interleukin (IL)-1β is induced by silica and functions as the key pro-inflammatory cytokine in this process. The Th17 response, which is induced by IL-1β, has been reported very important in chronic human lung inflammatory diseases. To elucidate the underlying mechanisms of IL-1β and IL-17 in silicosis, we used anakinra and an anti-IL-17 monoclonal antibody (mAb) to block the receptor of IL-1β (IL-RI) and IL-17, respectively, in a mouse model of silicosis. We observed increased IL-1β expression and an enhanced Th17 response after silica instillation. Treatment with an IL-1 type I receptor (IL-1RI) antagonist anakinra substantially decreased silica-induced lung inflammation and the Th17 response. Lung inflammation and the accumulation of inflammatory cells were attenuated in the IL-17-neutralized silicosis group. IL-17 may promote lung inflammation by modulating the differentiation of Th1 and regulatory T cells (Tregs) and by regulating the production of IL-22 and IL-1β during the lung inflammation of silicosis. Silica may induce IL-1β production from alveolar macrophages and promote inflammation by initiating a Th17 response via an IL-1β/IL-1RI-dependent mechanism. The Th17 response could induce lung inflammation during the pathogenesis of silicosis by regulating the homoeostasis of the Th immune responses and affecting the production of IL-22 and IL-1β. This study describes a potentially important inflammatory mechanism of silicosis that may bring about novel therapies for this inflammatory and fibrotic disease.
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