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Am J Physiol Lung Cell Mol Physiol 282: L237-L248, 2002; doi:10.1152/ajplung.00024.2001
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Vol. 282, Issue 2, L237-L248, February 2002

PM10-exposed macrophages stimulate a proinflammatory response in lung epithelial cells via TNF-alpha

L. A. Jiménez1, E. M. Drost1, P. S. Gilmour1, I. Rahman1, F. Antonicelli1, H. Ritchie1, W. MacNee1, and K. Donaldson2

1 Edinburgh Lung and the Environment Group Initiative/Colt Laboratories, Department of Medical and Radiological Sciences, University of Edinburgh, Edinburgh EH8 9AG; and 2 School of Life Sciences, Napier University, Edinburgh EH10 5DT, Scotland, United Kingdom

There is now considerable evidence for an association between the levels of particulate air pollution [particulate matter <10 µm in aerodynamic diameter (PM10)] and various adverse health endpoints. The release of proinflammatory mediators from PM10-exposed macrophages may be important in stimulating cytokine release from lung epithelial cells, thus amplifying the inflammatory response. A549 cells were treated with conditioned media from monocyte-derived macrophages stimulated with PM10, titanium dioxide (TiO2), or ultrafine TiO2. We demonstrate that only conditioned media from PM10-stimulated macrophages significantly increased nuclear factor-kappa B and activator protein-1 DNA binding, enhanced interleukin-8 (IL-8) mRNA levels as assessed by RT-PCR, and augmented IL-8 protein levels, over untreated controls. Furthermore, PM10-conditioned media also caused transactivation of IL-8 as determined by an IL-8-chloramphenicol acetyl transferase reporter. Analysis of these conditioned media revealed marked increases in tumor necrosis factor-alpha (TNF-alpha ) and protein levels and enhanced chemotactic activity for neutrophils. Preincubation of conditioned media with TNF-alpha -neutralizing antibodies significantly reduced IL-8 production. These data suggest that PM10-activated macrophages may amplify the inflammatory response by enhancing IL-8 release from lung epithelial cells, in part, via elaboration of TNF-alpha .

particulate matter; tumor necrosis factor-alpha ; nuclear factor-kappa B; cytokine networking; interleukin-8


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