You are here:
DIFFERENTIAL GENE EXPRESSION BY CHAPEL HILL FINE PARTICLES IN HUMAN ALVEOLAR MACHROPHAGES
Citation:
Huang, YuhChin T, Z. Li, J Carter, D. A. Schwartz, AND I. V. Yang. DIFFERENTIAL GENE EXPRESSION BY CHAPEL HILL FINE PARTICLES IN HUMAN ALVEOLAR MACHROPHAGES. Presented at American Thoracic Society Annual Conference, San Diego, CA, March 20 - 25, 2005.
Description:
Pollutant particles (PM) induce systemic and lung inflammation. Alveolar macrophages (AM) are one of the lung cells directly exposed to PM that may initiate these responses. In this study, we determined the gene expression profile induced by Chapel Hill fine particles (PM2.5) in human AM. AM were obtained from normal subjects by bronchoscopic lavage and incubated for 18 hours with or without 1 g/ml of PM2.5 collected in October of 2001. The RNAs were extracted and amplified with the Agilent low RNA input fluorescent linear amplification kit, and hybridized to the Agilent Human 1A(v1) microarrays (n = 6 for each group, dye flip replicates included). Differentially expressed genes were identified using the Significance Analysis for Microarray (SAM) algorithm with FDR at 10%. 34 and 43 genes were up- and down-regulated with treatment/control ratio > 1.5 or < 0.5 respectively. The top thirteen differentially expressed genes were confirmed by RT-PCR. Fourteen genes were involved in oxidative stress, including upregulation of metallothioneins, NCF1 (p47phox), CYP1B1, NQO1, MMP9, AMID, ATOX1 and downregulation of DHRS8 and HADHSC. Using the Database for Annotation, Visualization and Integrated Discovery (http://apps1.niaid.nih.gov/david/) (GOCharts), we found that the defense response and the response to pest/pathogen/parasite were the two biological processes with the most number of genes (10 and 8 respectively). The hierarchical clustering using the 77 genes completely separated PM2.5 from the control. These results indicate that exposure to Chapel Hill PM2.5 induced novel genes associated with oxidative stress and host defense in human AM. The gene expression profile may be used to identify genes and pathways involved in the biological response to ambient air pollutant. (Abstract does not reflect USEPA policy).