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1 School of Life Sciences, Napier University, Edinburgh, Scotland, United Kingdom
2 Particle Research Core, Institut fur Umweltmedizinische Forschung, Dusseldorf, Germany
3 Pulmonary Toxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Raleigh/Durham, North Carolina, USA
4 ELEGI Laboratory, University of Edinburgh, Edinburgh, Scotland, United Kingdom
* To whom correspondence should be addressed. E-mail: da.brown{at}napier.ac.uk.
Ultrafine particles are a component of particulate air pollution which have been suggested to be responsible for the health effects associated with elevations of this
pollutant. We have previously suggested that ultrafine particles, through the induction of oxidative stress may induce inflammation in the lung, thus exacerbating pre-existing illness in susceptible individuals. Alveolar macrophages are considered to play a key role in particle-mediated inflammation and lung disease. The effect of
ultrafine (Uf) particles on rat alveolar macrophages and human blood monocytes was investigated with reference to the roles of calcium and reactive oxygen species.
TNF-
protein release, intracellular calcium concentration, TNF- mRNA expression
and transcription factor activation were studied as end points after treatment of rat alveolar macrophages or peripheral blood monocytes. The calcium channel blocker
Verapamil, the intracellular calcium chelator BAPTA-AM, the calmodulin inhibitor W-7 and the antioxidants Trolox and Nacystelin (NAL) were included in combination
with Uf particles. Verapamil reduced the intracellular calcium concentration in rat alveolar macrophages on stimulation with Uf particles. This effect was also apparent with transcription factor AP-1 activation. All antagonists and antioxidants reduced the Ufstimulated
nuclear localisation of the p50 and p65 subunits of NF-
B in human monocytes. Verapamil, BAPTA-AM and NAL reduced the Uf-stimulated TNF- protein release whereas only Verapamil reduced Uf-stimulated mRNA expression in rat alveolar macrophages. In human monocytes, Verapamil, Trolox, BAPTA-AM and W-7 reduced Uf-stimulated TNF- protein release. These findings suggest that Uf particles may exert their pro-inflammatory effects by
modulating intracellular calcium concentrations, activation of transcription factors, and cytokine production through a reactive oxygen species-mediated mechanism.
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