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86962 
Journal Article 
Air pollution particles induce IL-6 gene expression in human airway epithelial cells via NF-kappaB activation 
Quay, JL; Reed, W; Samet, J; Devlin, RB 
1998 
Yes 
American Journal of Respiratory Cell and Molecular Biology
ISSN: 1044-1549
EISSN: 1535-4989 
19 
1 
98-106 
English 
9651185 
WOS:000074829600013 
#Fine particles in the air have been associated with increased mortality and morbidity. Particulate air pollution is a complex mixture which varies by region and includes a number of components including residual oil fly ash (ROFA), a byproduct of power plant and industry fuel-oil combustion. Human airway epithelial cells exposed to ROFA release inflammatory cytokines including interleukin (IL)-6, IL-8, and tumor necrosis factor. Expression of these genes is dependent upon pretranscriptional binding of cis regulatory elements, including nuclear factor 'kappa'B (NF-'kappa'B). To investigate the role of NF-'kappa'B in the particulate-induced IL-6 response, we exposed human airway epithelial cells (BEAS-2B) to ROFA in vitro. ROFA stimulated a time- and dose-dependent increase in IL-6 messenger RNA (mRNA), which was preceded by the activation of nuclear proteins binding to the NF-'kappa'B sequence motif in the IL-6 promoter. Transient transfection of BEAS-2B cells with the 5' promoter region of the IL-6 gene linked to a luciferase reporter gene confirmed that NF-B binding is necessary for the transcription of IL-6 mRNA. The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NF-'kappa'B may be mediated through reactive oxygen intermediates generated by transition metals found in ROFA. Activation of NF-'kappa'B may therefore be a critical first step in the inflammatory cascade following exposure to particles generated by oil combustion. 
Fuel Oils; DNA -- metabolism; Humans; Acetylcysteine -- pharmacology; Coal Ash; RNA, Messenger -- genetics; Epithelial Cells -- cytology; Promoter Regions, Genetic; Deferoxamine -- pharmacology; Epithelial Cells -- drug effects; RNA, Messenger -- metabolism; Transfection; Particulate Matter; Carbon -- toxicity; Cell Line; Free Radical Scavengers -- pharmacology; Bronchi -- cytology; Interleukin-6 -- genetics; Gene Expression Regulation; Bronchi -- metabolism; Bronchi -- drug effects; Air Pollutants -- toxicity; NF-kappa B -- metabolism; Metals -- toxicity 
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