Diesel exhaust activates redox-sensitive transcription factors and kinases in human airways
| Autor: | Anthony J. Frew, Susan J. Wilson, James M. Samet, Thomas Sandström, Ian Mudway, Jamshid Pourazar, Anders Blomberg, Ragnberth Helleday, Frank J. Kelly |
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| Rok vydání: | 2005 |
| Předmět: |
Adult
Male Pulmonary and Respiratory Medicine Diesel exhaust MAP Kinase Signaling System Physiology Inflammatory response Bronchi Biology p38 Mitogen-Activated Protein Kinases Epithelium Physiology (medical) Humans Transcription factor Vehicle Emissions Air Pollutants Kinase JNK Mitogen-Activated Protein Kinases Transcription Factor RelA Oxidation reduction Cell Biology Human airway Particulates Redox sensitive Cell biology Transcription Factor AP-1 Immunology Cytokines Female Inflammation Mediators Oxidation-Reduction Protein Kinases Transcription Factors |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 289:L724-L730 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.00055.2005 |
| Popis: | 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-α, 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 3] and air, immunohistochemical staining was used to quantify the expression of the transcription factors NF-κB (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-κB ( 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 |
| Databáze: | OpenAIRE |
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