ArticleParticle and fibre toxicology2010
NF-kappaB dependent and independent mechanisms of quartz-induced proinflammatory activation of lung epithelial cells.
Article in Particle and fibre toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 67 citations in OpenAlex.
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- Short and long-term associations between serum proteins linked to cardiovascular disease and particle exposure among constructions workers.Scandinavian journal of work, environment & health · 2023Article
- Profiling of metabolites, proteins, and protein phosphorylation in silica-exposed BEAS-2B epithelial cells.PloS one · 2023Article
- Time-Dependent Oxidative Alterations in Plasma and Lung Tissue after Meconium Aspiration in a Rabbit Model.Antioxidants (Basel, Switzerland) · 2022Article
- Exploring NFJournal of public health in Africa · 2022Article
- Gene Expression Profiling of Mono- and Co-Culture Models of the Respiratory Tract Exposed to Crystalline Quartz under Submerged and Air-Liquid Interface Conditions.International journal of molecular sciences · 2022Article
- 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
- Raspberry Ketones Attenuate Cyclophosphamide-Induced Pulmonary Toxicity in Mice through Inhibition of Oxidative Stress and NF-ΚB Pathway.Antioxidants (Basel, Switzerland) · 2020Article
- Evaluation of the NLRP3 Inflammasome Activating Effects of a Large Panel of TiONanomaterials (Basel, Switzerland) · 2020Article
- Article
- The puzzling issue of silica toxicity: are silanols bridging the gaps between surface states and pathogenicity?Particle and fibre toxicology · 2019Article
- Characteristics of surfactant proteins in tumorigenic and inflammatory lung lesions in rodents.Journal of toxicologic pathology · 2018Review
- Cerium oxide and barium sulfate nanoparticle inhalation affects gene expression in alveolar epithelial cells type II.Journal of nanobiotechnology · 2018Article
- Urban particulate matter (PM) suppresses airway antibacterial defence.Respiratory research · 2018Article
- Suppressive effects of the expectorant drug ambroxol hydrochloride on quartz-induced lung inflammation in F344 rats.Journal of toxicologic pathology · 2017Article
- Meconium-induced inflammation and surfactant inactivation: specifics of molecular mechanisms.Pediatric research · 2016Review
- Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells.Human molecular genetics · 2015Article
- Biomarker as a research tool in linking exposure to air particles and respiratory health.BioMed research international · 2015Review
- Pharmacologic suppression of inflammation by a diphenyldifluoroketone, EF24, in a rat model of fixed-volume hemorrhage improves survival.The Journal of pharmacology and experimental therapeutics · 2013Article
- Contrasting macrophage activation by fine and ultrafine titanium dioxide particles is associated with different uptake mechanisms.Particle and fibre toxicology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the initiation and progression of pulmonary inflammation, macrophages have classically been considered as a crucial cell type. However, evidence for the role of epithelial type II cells in pulmonary inflammation has been accumulating. In the current study, a combined in vivo and in vitro approach has been employed to investigate the mechanisms of quartz-induced proinflammatory activation of lung epithelial cells. In vivo, enhanced expression of the inflammation- and oxidative stress-related genes HO-1 and iNOS was found on the mRNA level in rat lungs after instillation with DQ12 respirable quartz. Activation of the classical NF-kappaB pathway in macrophages and type II pneumocytes was indicated by enhanced immunostaining of phospho-IkappaBalpha in these specific lung cell types. In vitro, the direct, particle-mediated effect on proinflammatory signalling in a rat lung epithelial (RLE) cell line was compared to the indirect, macrophage product-mediated effect. Treatment with quartz particles induced HO-1 and COX-2 mRNA expression in RLE cells in an NF-kappaB independent manner. Supernatant from quartz-treated macrophages rapidly activated the NF-kappaB signalling pathway in RLE cells and markedly induced iNOS mRNA expression up to 2000-fold compared to non-treated control cells. Neutralisation of TNFalpha and IL-1beta in macrophage supernatant did not reduce its ability to elicit NF-kappaB activation of RLE cells. In addition the effect was not modified by depletion or supplementation of intracellular glutathione. The results from the current work suggest that although both oxidative stress and NF-kappaB are likely involved in the inflammatory effects of toxic respirable particles, these phenomena can operate independently on the cellular level. This might have consequences for in vitro particle hazard testing, since by focusing on NF-kappaB signalling one might neglect alternative inflammatory pathways.
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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.