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In vivo endothelial transcriptomic responses to diesel engine exhaust are potentiated by hypercholesterolemia

ABSTRACT: By means of Operon V3 microarrrays, the in vivo, aortic endothelial transcriptomic responses to chronic (30 day) whole body exposure to diesel exhaust were assessed in wild type and Apo E (-/-) mice. The in vitro response of cultured Svec 4-10 cells exposed to a soluble extract extract of diesel engine particulate were similarly assessed.

ORGANISM(S): Mus musculus

PROVIDER: GSE13160 | GEO | 2008/12/15

SECONDARY ACCESSION(S): PRJNA109743

REPOSITORIES: GEO

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Transcriptomic Changes in the Nasal Epithelium Associated with Diesel Engine Exhaust Exposure

Project description:Diesel engine exhaust (DEE) is one of the major contributors to air pollution around the world, and exposure to DEE is associated with lung cancer and other airway diseases. Although recent studies have investigated the effects of exposure to DEE, the mechanisms by which it leads to lung cancer pathogenesis are not well understood. We have previously investigated the transcriptomic changes that occur due to exposure to cigarette smoke and burning of bituminous (smoky) as well as anthracite (smokeless) coal in the airway epithelium, and in this study we assess the gene expression alterations in the nasal epithelium that are associated with chronic DEE exposure of diesel engine factory workers to better understand which molecular changes may lead to pathogenesis of lung cancer.

2019-12-19 | GSE124267 | GEO

Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice II

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Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO). The lung cells were exposed 3 times to each combustion aerosol (DF or HFO). The duration of the exposure was 4h. The cells were seeded into transwell-inserts 24h before exposure. Within each exposure 3 transwell-inserts were exposed to the complete aerosol and 3 transwell-inserts were exposed to the filtered aerosol. Effects of the complete aerosol were referenced against the filtered aerosol to determine the effects of the aerosol particles.

2015-02-01 | E-GEOD-63962 | biostudies-arrayexpress

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Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice II

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Transcriptomic Changes in the Nasal Epithelium Associated with Diesel Engine Exhaust Exposure

Project description:Transcriptomic Changes in the Nasal Epithelium Associated with Diesel Engine Exhaust Exposure

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Murine lung: Control vs Diesel Exhaust Exposed

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Hypercholesterolemia potentiates aortic endothelial response to inhaled diesel exhaust.

Project description:BackgroundInhalation of diesel exhaust induces vascular effects including impaired endothelial function and increased atherosclerosis.ObjectiveTo examine the in vivo effects of subchronic diesel exhaust exposure on endothelial cell transcriptional responses in the presence of hypercholesterolemia.MethodsApoE (-/-) and ApoE (+/+) mice inhaled diesel exhaust diluted to particulate matter levels of 300 or 1000 μg/m³ vs. filtered air. After 30 days, endothelial cells were harvested from dispersed aortic cells by fluorescent-activated cell sorting (FACS). Relative mRNA abundance was evaluated by microarray analysis to measure strain-specific transcriptional responses in mice exposed to dilute diesel exhaust vs. filtered air.ResultsForty-nine transcripts were significantly dysregulated by >2.8-fold in the endothelium of ApoE (-/-) mice receiving diesel exhaust at 300 or 1000 μg/m³. These included transcripts with roles in plasminogen activation, endothelial permeability, inflammation, genomic stability, and atherosclerosis; similar responses were not observed in ApoE (+/+) mice.ConclusionsThe potentiation of diesel exhaust-related endothelial gene regulation by hypercholesterolemia helps to explain air pollution-induced vascular effects in animals and humans. The observed regulated transcripts implicate pathways important in the acceleration of atherosclerosis by air pollution.

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Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets.

Project description:BackgroundThe International Agency for Research on Cancer recently classified diesel engine exhaust (DEE) as a Group I carcinogen based largely on its association with lung cancer. However, the exposure-response relationship is still a subject of debate and the underlying mechanism by which DEE causes lung cancer in humans is not well understood.MethodsWe conducted a cross-sectional molecular epidemiology study in a diesel engine truck testing facility of 54 workers exposed to a wide range of DEE (ie, elemental carbon air levels, median range: 49.7, 6.1-107.7 µg/m(3)) and 55 unexposed comparable controls.ResultsThe total lymphocyte count (p=0.00044) and three of the four major lymphocyte subsets (ie, CD4+ T cells (p=0.00019), CD8+ T cells (p=0.0058) and B cells (p=0.017)) were higher in exposed versus control workers and findings were highly consistent when stratified by smoking status. In addition, there was evidence of an exposure-response relationship between elemental carbon and these end points (ptrends<0.05), and CD4+ T cell levels were significantly higher in the lowest tertile of DEE exposed workers compared to controls (p=0.012).ConclusionsOur results suggest that DEE exposure is associated with higher levels of cells that play a key role in the inflammatory process, which is increasingly being recognised as contributing to the aetiology of lung cancer.ImpactThis study provides new insights into the underlying mechanism of DEE carcinogenicity.

| S-EPMC6438624 | biostudies-literature

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