Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Mehrdad Arjomandi

PROVIDER: E-GEOD-58682 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness; Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 Âµm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) âinduced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naÃ¯ve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Experiment Overall Design: animals were treated by PBS, Oval albumin, PM, or both OVA/PM

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

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