Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of lung RNA from spontaneously hypertensive male rats after exposure to urban particulate matter (EHC-93)

ABSTRACT: We isolated total lung RNA from spontaneously hypertensive male rats 2â40 h after exposure to reference EHC-93. Three animals were exposed to EHC-93 in saline(10 mg/kg body weight) or saline at each time via intratracheal instillation or no instillation at all. RNA from different times was pooled for array hybridization as indicated.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Jeroen Pennings

PROVIDER: E-GEOD-1796 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression pattern in spontaneously hypertensive rats exposed to urban particulate matter (EHC-93).

Kooter I I Pennings J J Opperhuizen A A Cassee F F

Inhalation toxicology 20050101 1

Epidemiological studies show associations of short-term exposure to particulate matter with morbidity and mortality. Although many studies investigate the health effects of ambient particulate matter, the associated mechanisms, and the causality, they often focus on classical parameters. The objective of the present study was to gain insight into the roles of a wide range of genes in this process. Particular attention has been paid to immediate oxidative stress in the lung. We isolated total lun ...[more]

PMID: 15764483

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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 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced 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 naïve 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. Keywords: gene expression

Dataset Information

Transcription profiling of lung RNA from spontaneously hypertensive male rats after exposure to urban particulate matter (EHC-93)

Publications

Gene expression pattern in spontaneously hypertensive rats exposed to urban particulate matter (EHC-93).

Similar Datasets

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