ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Diesel exhaust particles override natural injury-limiting pathways in the lung.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. 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, 31 citations in OpenAlex.
- The Impact of the Reduction in Environmental Pollution during COVID-19 Lockdown on Healthy Individuals.Toxics · 2024Article
- Road tunnel-derived coarse, fine and ultrafine particulate matter: physical and chemical characterization and pro-inflammatory responses in human bronchial epithelial cells.Particle and fibre toxicology · 2022Article
- SARS-CoV-2 infection, COVID-19 pathogenesis, and exposure to air pollution: What is the connection?Annals of the New York Academy of Sciences · 2021Review
- Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro.Environmental research · 2021Article
- Exposure to diesel exhaust particles increases susceptibility to invasive pneumococcal disease.The Journal of allergy and clinical immunology · 2020Article
- DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling.Journal of virology · 2019Article
- Low dose of chlorine exposure exacerbates nasal and pulmonary allergic inflammation in mice.Scientific reports · 2018Article
- Multi-cellular human bronchial models exposed to diesel exhaust particles: assessment of inflammation, oxidative stress and macrophage polarization.Particle and fibre toxicology · 2018Article
- Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury.PloS one · 2015Article
- Inflammation-related effects of diesel engine exhaust particles: studies on lung cells in vitro.BioMed research international · 2013Review
- Roles of neutrophils in the regulation of the extent of human inflammation through delivery of IL-1 and clearance of chemokines.Journal of leukocyte biology · 2013Article
- The inflammasome in lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2012Review
- Pellino-1 selectively regulates epithelial cell responses to rhinovirus.Journal of virology · 2012Article
- Interleukin-1β regulates CXCL8 release and influences disease outcome in response to Streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages.Infection and immunity · 2012Article
- Diesel exhaust particle exposure in vitro alters monocyte differentiation and function.PloS one · 2012Article
- Effects of air pollutants on innate immunity: the role of Toll-like receptors and nucleotide-binding oligomerization domain-like receptors.The Journal of allergy and clinical immunology · 2012Review
- Role of interleukin-1 and MyD88-dependent signaling in rhinovirus infection.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Induction of effective inflammation in the lung in response to environmental and microbial stimuli is dependent on cooperative signaling between leukocytes and lung tissue cells. We explored how these inflammatory networks are modulated by diesel exhaust particles (DEP) using cocultures of human monocytes with epithelial cells. Cocultures, or monoculture controls, were treated with DEP in the presence or absence of LPS or flagellin. Production of cytokines was explored by Western blotting and ELISA; cell signaling was analyzed by Western blotting. Here, we show that responses of epithelial cells to DEP are amplified by the presence of monocytes. DEP amplified the responses of cellular cocultures to very low doses of TLR agonists. In addition, in the presence of DEP, the responses induced by LPS or flagellin were less amenable to antagonism by the physiological IL-1 antagonist, IL-1ra. This was paralleled by the uncoupling of IL-1 production and release from monocytes, potentially attributable to an ability of DEP to sequester or degrade extracellular ATP. These data describe a model of inflammation where DEP amplifies responses to low concentrations of microbial agonists and alters the nature of the inflammatory milieu induced by TLR agonists.
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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.