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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-
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-
(TNF-) and protein levels and enhanced
chemotactic activity for neutrophils. Preincubation of conditioned
media with TNF--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-.
particulate matter; tumor necrosis factor-; nuclear factor-B; cytokine networking; interleukin-8
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