ArticleClinical and experimental immunology2001
The influence of diesel exhaust particles on mononuclear phagocytic cell-derived cytokines: IL-10, TGF-beta and IL-1 beta.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 43 citations in OpenAlex.
- Long-Term Particulate Matter Exposure May Increase Risk of Chronic Rhinosinusitis WIth Nasal Polyposis: Results From an Exposure-Matched Study.International forum of allergy & rhinology · 2025Article
- Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024Review
- Article
- Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet.Particle and fibre toxicology · 2021Article
- Cancer Stem Cells: Emergent Nature of Tumor Emergency.Frontiers in genetics · 2018Article
- Variability in bioreactivity linked to changes in size and zeta potential of diesel exhaust particles in human immune cells.PloS one · 2014Article
- Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Pathogenesis and disease mechanisms of occupational asthma.Immunology and allergy clinics of North America · 2011Review
- The effect of air pollution on asthma and allergy.Current allergy and asthma reports · 2008Review
- Enhancement of acute lung injury related to bacterial endotoxin by components of diesel exhaust particles.Thorax · 2003Article
- Diesel fumes and the rising prevalence of atopy: an urban legend?Current allergy and asthma reports · 2003Review
- Inflammasome in the Pathogenesis of Pulmonary Diseases.Experientia supplementum (2012)Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Diesel exhaust particles (DEP) are known to modulate the production of cytokines associated with acute and chronic respiratory symptoms and allergic respiratory disease. Tolerance is an important mechanism through which the immune system can maintain nonresponsiveness to common environmental antigens. We examined the effect of DEP on IL-10 and TGF-beta, cytokines produced by macrophages and repressor (Tr-like) lymphocytes which influence tolerance. Human PBMCs (n = 22) were incubated with 1-100 ng/ml of DEP, and suboptimally primed with LPS. IL-10 gene expression was assessed by the S1 nuclease protection assay, and production of IL-10, TGF-beta, TNF-alpha, IL-1 beta and IL-4 stimulated CD23 was evaluated by ELISA after 24 and 48 h. The effect of the order of exposure to DEP and LPS was evaluated on IL-10 protein and mRNA in cells (1) preincubated with LPS followed by DEP, or (2) exposed first to DEP followed by LPS. IL-10 was further evaluated using benzo[a]pyrene and [alpha]naphthoflavone as a surrogate for the polyaromatic hydrocarbons (PAHs) adsorbed to DEP. Control cells were incubated with carbon black, without PAHs. In PBMCs exposed to DEP with LPS, or preincubated with LPS before DEP, IL-10 production and mRNA fall significantly. TGF-beta is similarly suppressed, IL-1 beta secretion is significantly stimulated, and IL-4 stimulated CD23 release rises in the atopic subjects. In contrast, when DEP is added prior to LPS, IL-10 production rises, and IL-1 beta falls to zero. These effects on IL-10 are reproduced with benzo[a]pyrene and reversed by the coaddition of [alpha]naphthoflavone, its known antagonist. The carbon black fraction has no effect on IL-10 production. The effect of DEP on IL-10 can be inhibitory or stimulatory, depending on the order of exposure to DEP and LPS. Pro-inflammatory cytokines and factors rise when IL-10 is inhibited, and are suppressed when IL-10 is stimulated. These results are duplicated with benzo[a]pyrene, suggesting that the PAH portion of the DEP is the active agent.
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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.