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Ozone Exposure Alters MicroRNA Expression Profiles in Humans

ABSTRACT: We set out to test the hypothesis that ozone inhalation exposure significantly alters miRNA expression profiles within the airway of humans. Adult human volunteers were exposed to 0.4 ppm ozone for two hours. Induced sputum samples were collected from each subject 48 hours pre-exposure and 6 hours post-exposure. Genome-wide miRNA expression profiles were evaluated using microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47977 | GEO | 2014/07/01

SECONDARY ACCESSION(S): PRJNA208519

REPOSITORIES: GEO

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Ozone Exposure Alters MicroRNA Expression Profiles in Humans

Project description:We set out to test the hypothesis that ozone inhalation exposure significantly alters miRNA expression profiles within the airway of humans. Adult human volunteers were exposed to 0.4 ppm ozone for two hours. Induced sputum samples were collected from each subject 48 hours pre-exposure and 6 hours post-exposure. Genome-wide miRNA expression profiles were evaluated using microarray analysis. Twenty healthy non-asthmatic adult subjects aged 18 – 37 years, with no history of smoking in the past 10 years, completed the study. The ozone exposures were conducted in an exposure chamber. Each subject was exposed to 0.4 ppm ozone for two hours while performing four 15-minute sessions of intermittent moderate exercise (expiratory minute ventilation, 30–40 L/min) on a treadmill, separated by 15 minutes of seated rest. Induced sputum samples were collected from each subject 48 hours pre-exposure and 6 hours post-exposure. RNA samples were homogenized in TRIzol, and extracted according to standard TRIzol protocol. RNA was labeled and hybridized to the Agilent Human miRNA Microarray (v1.0).

2014-07-01 | E-GEOD-47977 | biostudies-arrayexpress

Effects of blocking IL-17A on lung gene expression after ozone exposure in obese (db/db) mice

Project description:Obese mice have an augmented response to Ozone exposure (2 ppm for 3 hours and studied 24 hours later), including increase airway hyperresponsiveness and BAL inflammation when compared to WT ozone exposed mice. When IL-17A is block with systemic injected of IL-17A antibodies there is a decrease of response in the obese mice. To determine the mechanism of action, RNA was extracted from the lungs of IL-17A and Isotype injected ozone exposed obese mice and microarray analysis of gene expression was performed.

2016-05-24 | GSE81800 | GEO

Human Bronchoalveolar Lavage Cells Gene Expression After Exposure to Increasing Doses of Ozone

Project description:Ozone, the major component of air pollution, is an oxidant gas. Inhalation of high ambient levels of ozone causes oxidative stress and airway inflammation. To assess the biological responses of airway inflammatory cells to ozone-induced oxidative stress, we examined the gene expression of airway inflammatory cells in response to inhalation of ozone. Nineteen subjects, with and without asthma, were exposed to clean air (0 ppb), low (100ppb), and high (200ppb) ambient levels of ozone for 4 hours on three separate occasions in a climate-controlled chamber followed by bronchoscopy with bronchoalveolar lavage (BAL) 20 hours after the end of exposure in a repeated measure design. The BAL cells mRNA expression was examined using Affymetrix GeneChip Microarray.

2015-06-15 | E-GEOD-58682 | biostudies-arrayexpress

ozone-derived oxisterols impair lung macrophage phagocytosis via adduction of phagocytosis receptors

Project description:Inhalation of the amibient air polution ozone causes lung inflammation and can suppress host defense mechanisms, including impairing macrophage phagocytosis. Ozone reacts with cholesterol in the lung to form oxysterols, like secosterol A and secosterol B, which can form covalent adducts on cellular proteins. How oxysterol-protein adduction modifies the function of lung macrophages is unknown. Herein, we used a preoteomic screen to identify lung macrophage proteins that fomr adducts with ozone-derived oxysterols. Analysis show that the phagocytic receptor CD206 and CD64 formed adducts with secosterol A. Adduction of these receptors with ozone-derived oxysterols impaired ligand binding and corresponded with reduced macrophage phagocytosis. This work suggests a novle mechanism for the suppression of macrophage phagocytosis following ozone exposure through the generation of oxysterols and the formation of oxysterol-protein adducts on phagocytic receptors.

2020-07-18 | PXD019317 | Pride

Formaldehyde and Epigenetic Alterations: MicroRNA Changes in the Nasal Epithelium of Nonhuman Primates

2012-09-01 | GSE34978 | GEO

Human Bronchoalveolar Lavage Cells Gene Expression After Exposure to Increasing Doses of Ozone

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Role of Notch receptors in ozone induced lung injury in mice

Project description:Ozone is a highly toxic air pollutant and global health concern. Mechanisms of genetic susceptibility to ozone-induced lung inflammation are not completely understood. We hypothesized Notch3 and Notch4 are important determinants of susceptibility to ozone-induced lung inflammation. Wild type (WT), Notch3 (Notch3-/-) and Notch4 (Notch4-/-) knockout mice were exposed to ozone (0.3 ppm) or filtered air for 6-72 hours. Ozone increased bronchoalveolar lavage fluid (BALF) protein, a marker of lung permeability, in all genotypes, but significantly greater concentrations were found in Notch4-/- compared to WT and Notch3-/-. Significantly greater mean numbers of BALF neutrophils were found in Notch3-/- and Notch4-/- mice compared to WT mice after ozone. Expression of whole lung Tnf was significantly increased after ozone in all genotypes, and was significantly greater in Notch3-/- mice compared to WT. Statistical analyses of the transcriptome identified differentially expressed gene networks between WT and knockout mice basally and after ozone, and included Trim30, a member of the inflammasome pathway, and Traf6, an inflammatory signaling member. These novel findings are consistent with Notch3 and Notch4 as susceptibility genes for ozone-induced lung injury, and suggest that Notch receptors protect against innate immune inflammation. Wild-type, Notch3 knockout, and Notch4 knockout mice at 7-13 weeks of age were exposed continuously to air or 0.3 ppm ozone for 6, 24, or 48 hours. Three biological replicates from individual animals were included in each exposure group from each genotype and samples hybridized to the GeneChip Mouse Genome 430 2.0 array (Affymetrix).

2015-02-24 | E-GEOD-58244 | biostudies-arrayexpress

Epigenetics effects of formaldehyde inhalation exposure

Project description:We set out to test the hypothesis that formaldehyde inhalation exposure significantly alters miRNA expression profiles within the nasal epithelium of nonhuman primates. Here, cynomolgus macaques were exposed to 0, 2, and 6 ppm formaldehyde for 6 hours/day across two consecutive days. RNA was extracted from the nasal maxilloturbinate region, a direct target of formaldehyde inhalation exposure. Genome-wide miRNA expression levels were assessed using microarrays. Cynomolgus macaques (Macaca fascicularis) were exposed to 0, 2 and 6 ppm formaldehyde for 6 hours/day across two consecutive days using whole body exposure chambers. RNA was extracted from the nasal maxilloturbinate region, a direct target of formaldehyde inhalation exposure. Genome-wide miRNA expression levels were assessed using microarrays.

2012-09-01 | E-GEOD-34978 | biostudies-arrayexpress

Effect of adiponectin deficiency on pulmonary responses to subacute ozone exposure in mice

Project description:Adiponectin is an adipose-derived hormone with anti-inflammatory activity. Following subacute ozone exposure (0.3 ppm for 24-72 h), pulmonary neutrophilic inflammation is augmented in adiponectin deficient mice. The purpose of this study was to use microarrays to examine the impact of adiponectin deficiency on changes in pulmonary gene expression induced by ozone, a common air pollutant. Lungs were harvested from wildtype and mice that were genetically deficient in adiponectin. Mice were exposed either to room air or to ozone (0.3 ppm) for 72 h. RNA was extracted and microarray analysis of gene expression performed. Both male and female mice were used.

2013-08-27 | E-GEOD-50183 | biostudies-arrayexpress

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