ArticleToxicological sciences : an official journal of the Society of Toxicology2003
Induction of chemokines by low-dose intratracheal silica is reduced in TNFR I (p55) null mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Cytokine Profiles as Predictive Biomarkers of Disease Severity and Progression in Engineered Stone Silicosis: A Machine Learning Approach.Diagnostics (Basel, Switzerland) · 2025Article
- 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
- Effect of Pulmonary Inflammation by Surface Functionalization of Zinc Oxide Nanoparticles.Toxics · 2021Article
- Role of Nephronectin in Pathophysiology of Silicosis.International journal of molecular sciences · 2019Review
- A Pathological Study of Acute Pulmonary Toxicity Induced by Inhaled Kanto Loam Powder.International journal of molecular sciences · 2018Article
- Anti-TNFα therapy in inflammatory lung diseases.Pharmacology & therapeutics · 2017Review
- Role of tumor necrosis factor-α and its receptors in diesel exhaust particle-induced pulmonary inflammation.Scientific reports · 2017Article
- IL-10-Producing CD1dFrontiers in immunology · 2017Article
- The complex cascade of cellular events governing inflammasome activation and IL-1β processing in response to inhaled particles.Particle and fibre toxicology · 2016Review
- Differential innate immune cell signatures and effects regulated by toll-like receptor 4 during murine lung tumor promotion.Experimental lung research · 2016Article
- Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha.Alcoholism, clinical and experimental research · 2015Article
- Silica-induced chronic inflammation promotes lung carcinogenesis in the context of an immunosuppressive microenvironment.Neoplasia (New York, N.Y.) · 2013Article
- LC50 Determination of tert-Butyl Acetate using a Nose Only Inhalation Exposure in Rats.Toxicological research · 2010Article
- IL-1beta augments TNF-alpha-mediated inflammatory responses from lung epithelial cells.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2009Article
- The effects of interleukin-1beta in tumor necrosis factor-alpha-induced acute pulmonary inflammation in mice.Mediators of inflammation · 2009Article
- Suppressive oligodeoxynucleotides inhibit silica-induced pulmonary inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Regulation of caveolin-1 expression, nitric oxide production and tissue injury by tumor necrosis factor-alpha following ozone inhalation.Toxicology and applied pharmacology · 2008Article
- Signal transduction pathways of tumor necrosis factor--mediated lung injury induced by ozone in mice.American journal of respiratory and critical care medicine · 2007Article
- Silica-directed mast cell activation is enhanced by scavenger receptors.American journal of respiratory cell and molecular biology · 2007Article
- Cytokine expression in mice exposed to diesel exhaust particles by inhalation. Role of tumor necrosis factor.Particle and fibre toxicology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies suggest that tumor necrosis factor alpha (TNF-alpha) and the TNFRI (p55) and TNFRRII (p75) receptors mediate the pulmonary fibrotic response to silica. In order to further define the role of the TNFRI (p55) receptor in induction of profibrotic chemokines by low-dose silica/crystalline silica (50 micro g/50 micro l/mouse) or control diluent saline was instilled into the trachea of TNFRI gene ablated ((-/-)) and C57BL/6 (WT) control mice. Lung tissue was harvested and bronchoalveolar lavage (BAL) performed 24 h and 28 days following silica administration. Selected profibrotic chemokine mRNAs were quantified by ribonuclease protection assay, normalized to ribosomal protein L32 mRNA content and expressed relative to saline control treated lungs. Induction of MIP-1beta, MIP-1alpha, MIP-2, IP-10, and MCP-1 mRNAs was attenuated in the TNFRI(-/-) mice, in comparison to WT mice, particularly at 28 days after exposure. ELISA assays for MIP-1alpha and MIP-2 in homogenized lung tissue similarly demonstrated marked induction of both chemokines 24 h after silica treatment, which was persistent at 28 days in WT but not in TNFRI(-/-) mice. The percentage of BAL cells that was neutrophils was comparably increased in WT and RI(-/-) lungs at 24 h (49 +/- 12% vs. 46 +/- 10%) and 28 days (6.2 +/- 1.5% vs. 4.5 +/- 1%). The increase in total lavagable cells and BAL protein was also independent of strain. Histology revealed mild alveolitis without granuloma formation in both strains, slightly decreased in TNFRI(-/-). This study demonstrates an increase in pro-fibrotic chemokines in response to a single intratracheal exposure to crystalline silica that was sustained at 28 days after treatment in WT but not in TNFRI(-/-) mice. Silica dependent recruitment of neutrophils to the alveolar space and alveolar protein leak were, however, not altered by the absence of the TNF receptor.
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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.