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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 ; Sandstrom, Thomas

American journal of physiology. Lung cellular and molecular physiology, 2005-11, Vol.289 (5), p.L724-L730 [Periódico revisado por pares]

United States

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Diesel exhaust activates redox-sensitive transcription factors and kinases in human airways
Autor: Pourazar, Jamshid ; Mudway, Ian S ; Samet, James M ; Helleday, Ragnberth ; Blomberg, Anders ; Wilson, Susan J ; Frew, Anthony J ; Kelly, Frank J ; Sandstrom, Thomas
Assuntos: Adult ; Air Pollutants - toxicity ; Bronchi - drug effects ; Bronchi - metabolism ; Cytokines - biosynthesis ; Epithelium - drug effects ; Epithelium - metabolism ; Female ; Humans ; Inflammation Mediators - metabolism ; JNK Mitogen-Activated Protein Kinases - metabolism ; Male ; MAP Kinase Signaling System - drug effects ; Oxidation-Reduction ; p38 Mitogen-Activated Protein Kinases - metabolism ; Protein Kinases - metabolism ; Transcription Factor AP-1 - metabolism ; Transcription Factor RelA - metabolism ; Transcription Factors - metabolism ; Vehicle Emissions - toxicity
É parte de: American journal of physiology. Lung cellular and molecular physiology, 2005-11, Vol.289 (5), p.L724-L730
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: 1 Department of Respiratory Medicine and Allergy, University Hospital, Umeå, 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, United States Environmental Protection Agency, Chapel Hill, North Carolina; and 4 Allergy and Inflammation Research, School of Medicine, University of Southampton, Southampton, United Kingdom Submitted 28 January 2005 ; accepted in final form 3 March 2005 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- , 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 µm, 300 µg/m 3 ] and air, immunohistochemical staining was used to quantify the expression of the transcription factors NF- B (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- 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 + 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. particulate matter Address for reprint requests and other correspondence: T. Sandström, Dept. of Respiratory Medicine and Allergy, Univ. Hospital, SE-901 85 Umeå, Sweden (e-mail: thomas.sandstrom{at}lung.umu.se )
Editor: United States
Idioma: Inglês;Sueco

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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 ; Sandstrom, Thomas

United States

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