Cigarette Smoke-Induced Reactive Oxygen Species (ROS) Production In Human Airway Epithelial Cells Is Calcium And NADPH-Oxidase (NOX) Dependent

2012 ◽  
Author(s):  
Yun Lin ◽  
Nicholas Hoffman ◽  
Mark Aksoy ◽  
Madesh Muniswamy ◽  
Steven Kelsen
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Cigarette Smoke ◽  
Reactive Oxygen ◽  
Airway Epithelial Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Airway Epithelial ◽  
Human Airway

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.

scholarly journals Production of Reactive Oxygen Species Is Turned On and Rapidly Shut Down in Epithelial Cells Infected with Chlamydia trachomatis

2009 ◽  
Vol 78 (1) ◽  
pp. 80-87 ◽  
Author(s):  
Gaëlle Boncompain ◽  
Benoît Schneider ◽  
Cédric Delevoye ◽  
Odile Kellermann ◽  
Alice Dautry-Varsat ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Regulatory Subunit ◽  
Developmental Cycle ◽  
Ros Production ◽  
Oxygen Species ◽  
Cell Defense

ABSTRACT Reactive oxygen species (ROS) are many-faceted compounds involved in cell defense against pathogens, as well as in cell signaling. Their involvement in the response to infection in epithelial cells remains poorly documented. Here, we investigated the production of ROS during infection with Chlamydia trachomatis, a strict intracellular pathogen, in HeLa cells. C. trachomatis induced a transient increase in the ROS level within a few hours, followed by a return to basal level 9 hours after infection. At this time point, the host enzyme dedicated to ROS production, NADPH oxidase, could no longer be activated by external stimuli, such as interleukin-1β. In addition, Rac, a regulatory subunit of the NADPH oxidase complex, was relocated to the membrane of the compartment in which the bacteria develop, the inclusion, while other subunits were not. Altogether, these results indicate that C. trachomatis infection elicits the production of ROS and that the bacteria rapidly target the activity of NADPH oxidase to shut it down. Prevention of ROS production at the onset of the bacterial developmental cycle might delay the host response to infection.

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