The University of Southampton
University of Southampton Institutional Repository

Diesel exhaust activates redox-sensitive transcription factors and kinases in human airways

Pourazar, Jamshid, Mudway, Ian S., Samet, James M., Helleday, Ragnberth, Blomberg, Anders, Wilson, Susan J., Frew, Anthony J., Kelly, Frank J. and Sandström, Thomas (2005) Diesel exhaust activates redox-sensitive transcription factors and kinases in human airways American Journal of Physiology. Lung Cellular and Molecular Physiology, 289, (5), L724-L730. (doi:10.1152/ajplung.00055.2005). (PMID:16214822).

Record type: Article


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 [particulates with a mass median diameter of <10 mum, 300 microg/m3] and air, immunohistochemical staining was used to quantify the expression of the transcription factors NF-kappaB (p65) and AP-1 (c-jun and c-fos), as well their upstream MAPKs, p38 and JNK, in the bronchial epithelium. In addition, phosphorylation of tyrosine residues was examined. DE induced a significant increase in the nuclear translocation of NF-kappaB (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 + nuclear) immunostaining of phosphorylated p38 (P = 0.03). A significant increase in nuclear phosphorylated tyrosine 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 proinflammatory cytokines.

Full text not available from this repository.

More information

Published date: March 2005


Local EPrints ID: 190917
ISSN: 1040-0605
PURE UUID: 48798489-d828-44de-aa38-b64193615c08

Catalogue record

Date deposited: 16 Jun 2011 13:41
Last modified: 18 Jul 2017 11:36

Export record



Author: Jamshid Pourazar
Author: Ian S. Mudway
Author: James M. Samet
Author: Ragnberth Helleday
Author: Anders Blomberg
Author: Susan J. Wilson
Author: Anthony J. Frew
Author: Frank J. Kelly
Author: Thomas Sandström

University divisions

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton:

ePrints Soton supports OAI 2.0 with a base URL of

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.