ToxSci Advance Access originally published online on August 13, 2004
Toxicological Sciences 2004 82(1):88-96; doi:10.1093/toxsci/kfh248
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Toxicological Sciences vol. 82 no. 1 © Society of Toxicology 2004; all rights reserved.
Inflammatory Cytokines and Cell Death in BEAS-2B Lung Cells Treated with Soil Dust, Lipopolysaccharide, and Surface-Modified Particles
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, 84112–5820
Received April 1, 2004; accepted July 15, 2004
Cultured human lung epithelial cells (BEAS-2B) were treated in vitro with PM2.5-enriched particles of soil-derived mineral dust from nine sites in the western United States. The particle samples simulate windblown dust and vehicle-generated emissions from unpaved roads. Five of the sites yielded relatively benign dust. Particles from three sites caused IL-6 release when cells were treated for 24 h at doses from 20 to 80 µg/cm2, and particles from one site were highly cytotoxic. The particle components or characteristics that caused the IL-6 release were stable at temperatures below 150°C, but were inactivated by treatment at 300–550°C. The active factors were also associated predominantly with the insoluble fraction, and were partially attenuated by leaching with aqueous and organic solvents. The IL-6 release caused by the particles was much greater than the cytokine response to either lipopolysaccharide (LPS) or to surrogate particles of titanium dioxide mixed with LPS, suggesting that endotoxin was not a major factor in the inflammatory response. The release of IL-8 in response to particle treatment was qualitatively similar to the IL-6 response, but release of TNF-
was not detected at the 24-h time point. The combined results support the hypothesis that some ambient dusts from geological sources can cause cell death and cytokine release in a lung cell line that is widely used as an in vitro model to study mechanisms of environmental respiratory injury.
Key Words: geological dust; physical treatment; cell culture; interleukin-6; IL-6; interleukin-8; IL-8; endotoxin; vanilloid receptor.
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