ArticleEnvironmental health perspectives2005
Time course of gene expression of inflammatory mediators in rat lung after diesel exhaust particle exposure.
Article in Environmental health perspectives, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 51 citations in OpenAlex.
- Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice.Toxicological research · 2024Article
- An Exploratory Study of the Relationships Between Diesel Engine Exhaust Particle Inhalation, Pulmonary Inflammation and Anxious Behavior.International journal of environmental research and public health · 2021Article
- Occupational exposure to diesel engine exhaust and alterations in immune/inflammatory markers: a cross-sectional molecular epidemiology study in China.Carcinogenesis · 2017Article
- MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis.Scientific reports · 2015Article
- Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury.PloS one · 2015Article
- Metabolic consequences of interleukin-6 challenge in developing neurons and astroglia.Journal of neuroinflammation · 2014Article
- A comparative study of lung toxicity in rats induced by three types of nanomaterials.Nanoscale research letters · 2013Article
- Low dose theophylline showed an inhibitory effect on the production of IL-6 and IL-8 in primary lung fibroblast from patients with COPD.Mediators of inflammation · 2012Article
- Diesel exhaust particles modulate the tight junction protein occludin in lung cells in vitro.Particle and fibre toxicology · 2009Article
- Diesel exhaust particles induce oxidative stress, proinflammatory signaling, and P-glycoprotein up-regulation at the blood-brain barrier.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008Article
- Proteomic analysis of bronchoalveolar lavage fluid: effect of acute exposure to diesel exhaust particles in rats.Environmental health perspectives · 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diesel exhaust particles (DEPs) at three concentrations (5, 35, and 50 mg/kg body weight) were instilled into rats intratracheally. We studied gene expression at 1, 7, and 30 days postexposure in cells obtained by bronchoalveolar lavage (BAL) and in lung tissue. Using real-time reverse transcriptase-polymerase chain reaction (RT-PCR), we measured the mRNA levels of eight genes [interleukin (IL)-1beta, IL-6, IL-10, iNOS (inducible nitric oxide synthase), MCP-1 (monocyte chemoattractant protein-1), MIP-2 (macrophage inflammatory protein-2), TGF-beta1 (transforming growth factor-beta1), and TNF-alpha (tumor necrosis factor-alpha )] in BAL cells and four genes [IL-6, ICAM-1 (intercellular adhesion molecule-1), GM-CSF (granulocyte/macrophage-colony stimulating factor), and RANTES (regulated upon activation normal T cell expressed and secreted)] in lung tissue. In BAL cells on day 1, high-dose exposure induced a significant up-regulation of IL-1beta, iNOS, MCP-1, and MIP-2 but no change in IL-6, IL-10, TGF-beta1, and TNF-alpha mRNA levels. There was no change in the mRNA levels of IL-6, RANTES, ICAM-1, and GM-CSF in lung tissue. Nitric oxide production and levels of MCP-1 and MIP-2 were increased in the 24-hr culture media of alveolar macrophages (AMs) obtained on day 1. IL-6, MCP-1, and MIP-2 levels were also elevated in the BAL fluid. BAL fluid also showed increases in albumin and lactate dehydrogenase. The cellular content in BAL fluid increased at all doses and at all time periods, mainly due to an increase in polymorphonuclear leukocytes. In vitro studies in AMs and cultured lung fibroblasts showed that lung fibroblasts are a significant source of IL-6 and MCP-1 in the lung.
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