ArticleInternational journal of medical sciences2018
Regulation of TLR4 in silica-induced inflammation: An underlying mechanism of silicosis.
Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 45 citations in OpenAlex.
- Global scenario of silica-associated diseases: A review on emerging pathophysiology of silicosis and potential therapeutic regimes.Toxicology reports · 2025Review
- Integration of serum pharmacochemistry with network pharmacology to reveal the potential mechanism of Yangqing Chenfei formula for the treatment of silicosis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Distinct Pro-Inflammatory Mechanisms Elicited by Short and Long Amosite Asbestos Fibers in Macrophages.International journal of molecular sciences · 2023Article
- Baicalin alleviates silica-induced lung inflammation and fibrosis by inhibiting TLR4/NF-?B pathway in rats.Physiological research · 2023Article
- Gasdermin D membrane pores orchestrate IL-1α secretion from necrotic macrophages after NFS-rich silica exposure.Archives of toxicology · 2023Article
- Article
- Caveolin-1 negatively regulates inflammation and fibrosis in silicosis.Journal of cellular and molecular medicine · 2022Article
- Acute Silica Exposure Triggers Pulmonary Inflammation Through Macrophage Pyroptosis: An Experimental Simulation.Frontiers in immunology · 2022Article
- Investigation of MicroRNA and transcription factor mediated regulatory network for silicosis using systems biology approach.Scientific reports · 2021Article
- Macrophage Autophagy and Silicosis: Current Perspective and Latest Insights.International journal of molecular sciences · 2021Review
- Ac-SDKP Attenuates Activation of Lung Macrophages and Bone Osteoclasts in Rats Exposed to Silica by Inhibition of TLR4 and RANKL Signaling Pathways.Journal of inflammation research · 2021Article
- Occupational Cement Dust Exposure and Inflammatory Nemesis: Bangladesh Relevance.Journal of inflammation research · 2021Article
- Biological effects of inhaled hydraulic fracturing sand dust. III. Cytotoxicity and pro-inflammatory responses in cultured murine macrophage cells.Toxicology and applied pharmacology · 2020Article
- MCPIP1 RNase and Its Multifaceted Role.International journal of molecular sciences · 2020Review
- DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure.Environmental science and pollution research international · 2020Article
- MyD88 regulates a prolonged adaptation response to environmental dust exposure-induced lung disease.Respiratory research · 2020Article
- Comparative Analysis of Global Gene Expression and Complement Components Levels in Umbilical Cord Blood from Preterm and Term Neonates: Implications for Significant Downregulation of Immune Response Pathways related to Prematurity.International journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is an incurable lung disease affecting millions of workers in hazardous occupations. It is caused by chronic exposure to the dust that contains free crystalline silica. Silica-induced lung damage occurs by several main mechanisms including cell death by apoptosis, fibrosis and production of cytokines. However, the signal pathways involved in these mechanisms are not fully characterized. In this study, the toll-like receptor 4 (TLR4)-related signal pathway was examined in silica-treated U937-differentiated macrophages. The expression level of TLR4 was measured by both quantitative PCR and Western blot. Confirmation of the involvement of MyD88/TIRAP and NFκB p65 cascade was performed by Western blot. The secretion of cytokines IL-1β, IL-6, IL-10 and TNFα was measured by enzyme-linked immunosorbent assay. Our results showed that TLR4 and related MyD88/TIRAP pathway was associated with silica-exposure in U937-differentiated macrophages. Protein expression of TLR4, MyD88 and TIRAP was upregulated when the U937-differentiated macrophages were exposed to silica. However, the upregulation was attenuated when TLR4 inhibitor, TAK-242 was present. At different incubation times of silica exposure, it was found that NFκB p65 cascade was activated at 10-60 minutes. Release of cytokines IL-1β, IL-6, IL-10 and TNFα was induced by silica exposure and the induction of IL-1β, IL-6 and TNFα was suppressed by the addition of TAK-242. In conclusion, our study demonstrated that TLR4 and related MyD88/TIRAP pathway was involved in silica-induced inflammation in U937-differentiated macrophages. Downstream NFκB p65 cascade was activated within 1 hour when the U937-differentiated macrophages were exposed to silica. The better understanding of early stage of silica-induced inflammatory process may help to develop earlier diagnosis of silicosis.
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