Diesel exhaust particles induce an inflammatory response in airway epithelial cells: Involvement of reactive oxygen species

BioFactors ◽  
2002 ◽  
Vol 16 (1-2) ◽  
pp. 15-17 ◽  
Author(s):  
V. Bonvallot ◽  
A. Baulig ◽  
S. Boland ◽  
F. Marano ◽  
A. Baeza
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Diesel Exhaust ◽  
Reactive Oxygen ◽  
Airway Epithelial Cells ◽  
Diesel Exhaust Particles ◽  
Oxygen Species ◽  
Airway Epithelial ◽  
Exhaust Particles

Involvement of reactive oxygen species in the metabolic pathways triggered by diesel exhaust particles in human airway epithelial cells

2003 ◽  
Vol 285 (3) ◽  
pp. L671-L679 ◽  
Author(s):  
Augustin Baulig ◽  
Michèle Garlatti ◽  
Véronique Bonvallot ◽  
Alexandre Marchand ◽  
Robert Barouki ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Ros Production ◽  
Oxygen Species ◽  
Expression Of Genes ◽  
Exhaust Particles ◽  
Nrf2 Transcription Factor

Diesel exhaust particles (DEP) induce a proinflammatory response in human bronchial epithelial cells (16HBE) characterized by the release of proinflammatory cytokines after activation of transduction pathways involving MAPK and the transcription factor NF-κB. Because cellular effects induced by DEP are prevented by antioxidants, they could be mediated by reactive oxygen species (ROS). Using fluorescent probes, we detected ROS production in bronchial and nasal epithelial cells exposed to native DEP, organic extracts of DEP (OE-DEP), or several polyaromatic hydrocarbons. Carbon black particles mimicking the inorganic part of DEP did not increase ROS production. DEP and OE-DEP also induced the expression of genes for phase I [cytochrome P-450 1A1 (CYP1A1)] and phase II [NADPH quinone oxidoreductase-1 (NQO-1)] xenobiotic metabolization enzymes, suggesting that DEP-adsorbed organic compounds become bioavailable, activate transcription, and are metabolized since the CYP1A1 enzymatic activity is increased. Because NQO-1 gene induction is reduced by antioxidants, it could be related to the ROS generated by DEP, most likely through the activation of the stress-sensitive Nrf2 transcription factor. Indeed, DEP induced the translocation of Nrf2 to the nucleus and increased protein nuclear binding to the antioxidant responsive element. In conclusion, we show that DEP-organic compounds generate an oxidative stress, activate the Nrf2 transcription factor, and increase the expression of genes for phase I and II metabolization enzymes.

The role of iron in reactive oxygen species generation from diesel exhaust particles

2006 ◽  
Vol 20 (6) ◽  
pp. 851-857 ◽  
Author(s):  
Sungjo Park ◽  
Haeyun Nam ◽  
Namhyun Chung ◽  
Jung-Duck Park ◽  
Young Lim
Keyword(s):  
Reactive Oxygen Species ◽  
Diesel Exhaust ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Diesel Exhaust Particles ◽  
Oxygen Species ◽  
Exhaust Particles

scholarly journals Lipid-soluble components in cigarette smoke induce mitochondrial production of reactive oxygen species in lung epithelial cells

2009 ◽  
Vol 297 (1) ◽  
pp. L109-L114 ◽  
Author(s):  
Marco van der Toorn ◽  
Delaram Rezayat ◽  
Henk F. Kauffman ◽  
Stephan J. L. Bakker ◽  
Rijk O. B. Gans ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Gaseous Phase ◽  
Mitochondrial Function ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Airway Epithelial Cells ◽  
Oxygen Species ◽  
Airway Epithelial

Reactive oxygen species (ROS) present in cigarette smoke (CS) are thought to contribute to the development of COPD. Although CS-ROS can hardly enter airway epithelial cells, and certainly not the circulation, systemic levels of ROS have been found to be elevated in COPD patients. We hypothesize that lipophilic components present in CS can enter airway epithelial cells and increase intracellular ROS production by disturbing mitochondrial function. Different airway epithelial cells were exposed to CS extract (CSE), hexane-treated CSE (CSE without lipophilic components), gaseous-phase CS, and water-filtered CS (gaseous-phase CS without ROS). Mitochondrial membrane potential (Δψm) and ATP levels were assessed using the bronchial epithelial cell line Beas-2b. ROS generation measured directly by DCF fluorescence and indirectly by measuring free thiol groups (-SH) upon exposure to CS was assessed using lung alveolar epithelial cells devoid of functional mitochondria (A549-ρ0), with normal A549 cells serving as controls. In Beas-2b cells, CSE (4 h) caused a dose-dependent decrease in Δψm and ATP levels, whereas hexane-treated CSE did not. DCF fluorescence in A549 cells increased in response to CSE, whereas this was not the case in A549-ρ0 cells. Exposure of A549 cells to CS resulted in a rapid decrease in free -SH, whereas exposure to ROS-depleted CS only resulted in a delayed decrease. This delayed decrease was less pronounced in A549-ρ0 cells. Lipophilic components in CS disturb mitochondrial function, which contributes to increased intracellular generation of ROS. Our results are of importance in understanding the systemic effects of smoking observed in patients with COPD.

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