ArticleParticle and fibre toxicology2008
IL-1beta differently involved in IL-8 and FGF-2 release in crystalline silica-treated lung cell co-cultures.
Article in Particle and fibre toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 62 citations in OpenAlex.
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- Plasma Cytokine Profiling Reveals Differences between Silicotic Patients with Simple Silicosis and Those with Progressive Massive Fibrosis Caused by Engineered Stone.International journal of molecular sciences · 2023Article
- Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review.Nanomaterials (Basel, Switzerland) · 2022Review
- Comparing α-Quartz-Induced Cytotoxicity and Interleukin-8 Release in Pulmonary Mono- and Co-Cultures Exposed under Submerged and Air-Liquid Interface Conditions.International journal of molecular sciences · 2022Article
- Pro-inflammatory effects of crystalline- and nano-sized non-crystalline silica particles in a 3D alveolar model.Particle and fibre toxicology · 2020Article
- Genome-wide DNA methylation analysis in lung fibroblasts co-cultured with silica-exposed alveolar macrophages.Respiratory research · 2017Article
- Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells.Human molecular genetics · 2015Article
- Immune Homeostasis in Epithelial Cells: Evidence and Role of Inflammasome Signaling Reviewed.Journal of immunology research · 2015Review
- Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.Journal of cellular and molecular medicine · 2014Article
- Silica induces NLRP3 inflammasome activation in human lung epithelial cells.Particle and fibre toxicology · 2013Article
- Differences in gene expression and cytokine production by crystalline vs. amorphous silica in human lung epithelial cells.Particle and fibre toxicology · 2012Article
- The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma.Comparative and functional genomics · 2012Article
- The nanosilica hazard: another variable entity.Particle and fibre toxicology · 2010Review
- Characterization of pentraxin 3 in the horse and its expression in airways.Veterinary researchArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhalation of crystalline silica particles is in humans associated with inflammation and development of fibrosis. The aim of the present study was to investigate the effect of crystalline silica on the release of the fibrosis- and angiogenesis-related mediator FGF-2 and the pro-inflammatory mediator IL-8, and how IL-1beta and TNF-alpha were involved in this release from various mono- and co-cultures of monocytes, pneumocytes and endothelial cells.
resultsSilica exposure induced an increase of IL-8 release from monocytes and from pneumocytes alone, and the FGF-2 level in the medium increased upon silica exposure of pneumocytes. Both the responses were enhanced in non-contact co-cultures with endothelial cells. The FGF-2 release seemed to increase with the silica-induced decrease in the number of pneumocytes. The release of IL-8 and FGF-2 was partially suppressed in cultures with pneumocytes in contact with monocytes compared to non-contact cultures. Treatment with anti-TNF-alpha and the IL-1 receptor antagonist revealed that release of IL-1beta, and not TNF-alpha, from monocytes dominated the regulation of IL-8 release in co-cultures. For release of FGF-2, IL-1ra was without effect. However, exogenous IL-1beta reduced the FGF-2 levels, strongly elevated the FGF-2-binding protein PTX3, and prevented the reduction in the number of pneumocytes induced by silica.
conclusionIL-1beta seems to be differently involved in the silica-induced release of IL-8 and FGF-2 in different lung cell cultures. Whereas the silica-induced IL-8 release is regulated via an IL-1-receptor-mediated mechanism, IL-1beta is suggested only indirectly to affect the silica-induced FGF-2 release by counteracting pneumocyte loss. Furthermore, the enhanced IL-8 and FGF-2 responses in co-cultures involving endothelial cells show the importance of the interaction between different cell types and may suggest that both these mediators are important in angiogenic or fibrogenic processes.
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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.