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Am J Physiol Lung Cell Mol Physiol (March 4, 2005). doi:10.1152/ajplung.00055.2005
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Submitted on January 28, 2005
Accepted on March 3, 2005

Diesel Exhaust Activates Redox Sensitive Transcription Factors and Kinases in Human Airways

Jamshid Pourazar1, Ian S. Mudway2, James M. Samet3, Ragnberth Helleday1, Anders Blomberg1, Susan J. Wilson4, Anthony J. Frew4, Frank J. Kelly2, and Thomas Sandstrom1*

1 Department of Respiratory Medicine and Allergy, Umea University, Umea, Sweden
2 Lung Biology, School of Health and Life Sciences, King's College London, London, United Kingdom
3 Human Studies Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, NC, USA
4 Allergy&Inflammation Research, School of Medicine, University of Southampton, Southampton, United Kingdom

* To whom correspondence should be addressed. E-mail: thomas.sandstrom{at}lung.umu.se.

Diesel exhaust (DE) is a major component of airborne particulate matter. In previous studies we have described the acute inflammatory response of the human airway to inhaled DE. This was characterized by neutrophil, mast cell and lymphocyte infiltration into the bronchial mucosa with enhanced epithelial expression of IL-8, Gro-{alpha} and IL-13. In the present study, we investigated whether redox-sensitive transcription factors were activated as a consequence of DE exposure, consistent with oxidative stress triggering airway inflammation. In archived biopsies from 15 healthy subjects exposed to DE (PM10, 300µg/m3) and air, immunohistochemical staining was used to quantify the expression of the transcription factors NF{kappa}B (p65) and AP-1 (c-jun and c-fos), as well their upstream mitogen activated protein kinases (MAPKs), p38 and JNK in the bronchial epithelium. In addition, phosphorylation of tyrosine residues (Tyr) was examined. DE induced a significant increase in the nuclear translocation of NF{kappa}B (p=0.02), AP-1 (p=0.02), phosphorylated-JNK (p=0.04) and phosphorylated-p38 (p=0.01), as well as an increase in total (cytoplasmic plus nuclear) immunostaining of phosphorylated-p38 (p=0.03). A significant increase in nuclear phosphorylated Tyr was also observed (p<0.05). These observations demonstrate that DE activates redox sensitive transcription factors in vivo consistent with oxidative stress triggering the increased synthesis of pro-inflammatory cytokines.




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