Superoxide dismutase moderates basal and induced bacterial adherence and interleukin-8 expression in airway epithelial cells

2004 ◽  
Vol 287 (6) ◽  
pp. L1199-L1206 ◽  
Author(s):  
Yuko Arita ◽  
Ansamma Joseph ◽  
Hshi-Chi Koo ◽  
Yuchi Li ◽  
Thomas A. Palaia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Epithelial Cells ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Bacterial Adherence ◽  
Interleukin 8 ◽  
Lung Epithelial Cells ◽  
Oxygen Species ◽  
Airway Epithelial

Bacterial infection of the tracheobronchial tree is a frequent, serious complication in patients receiving treatment with oxygen and mechanical ventilation, resulting in increased morbidity and mortality. Using human airway epithelial cell culture models, we examined the effect of hyperoxia on bacterial adherence and the expression of interleukin-8 (IL-8), an important mediator involved in the inflammatory process. A 24-h exposure to 95% O2increased Pseudomonas aeruginosa (PA) adherence 57% in A549 cells ( P < 0.01) and 115% in 16HBE cells ( P < 0.01) but had little effect on Staphylococcus aureus (SA) adherence. Exposure to hyperoxia, followed by a 1-h incubation with SA, further enhanced PA adherence ( P < 0.01), suggesting that hyperoxia and SA colonization may enhance the susceptibility of lung epithelial cells to gram-negative infections. IL-8 expression was also increased in cells exposed to both hyperoxia and PA. Stable or transient overexpression of manganese superoxide dismutase reduced both basal and stimulated levels of PA adherence and IL-8 levels in response to exposure to either hyperoxia or PA. These data indicate that hyperoxia increases susceptibility to infection and that the pathways are mediated by reactive oxygen species. Therapeutic intervention strategies designed to prevent accumulation of intracellular reactive oxygen species may reduce opportunistic pulmonary infections.

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 Cyclic mechanical strain increases reactive oxygen species production in pulmonary epithelial cells

2005 ◽  
Vol 289 (5) ◽  
pp. L834-L841 ◽  
Author(s):  
Kenneth E. Chapman ◽  
Scott E. Sinclair ◽  
Daming Zhuang ◽  
Aviv Hassid ◽  
Leena P. Desai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Cell Line ◽  
Primary Cultures ◽  
Reactive Oxygen ◽  
Lung Epithelial Cells ◽  
Alveolar Type ◽  
Ros Production ◽  
Oxygen Species ◽  
Type Ii

Overdistention of lung tissue during mechanical ventilation may be one of the factors that initiates ventilator-induced lung injury (VILI). We hypothesized that cyclic mechanical stretch (CMS) of the lung epithelium is involved in the early events of VILI through the production of reactive oxygen species (ROS). Cultures of an immortalized human airway epithelial cell line (16HBE), a human alveolar type II cell line (A549), and primary cultures of rat alveolar type II cells were cyclically stretched, and the production of superoxide (O2−) was measured by dihydroethidium fluorescence. CMS stimulated increased production of O2− after 2 h in each type of cell. 16HBE cells exhibited no significant stimulation of ROS before 2 h of CMS (20% strain, 30 cycles/min), and ROS production returned to control levels after 24 h. Oxidation of glutathione (GSH), a cellular antioxidant, increased with CMS as measured by a decrease in the ratio of the reduced GSH level to the oxidized GSH level. Strain levels of 10% did not increase O2− production in 16HBE cells, whereas 15, 20, and 30% significantly increased generation of O2−. Rotenone, a mitochondrial complex I inhibitor, partially abrogated the stretch-induced generation of O2− after 2 h CMS in 16HBE cells. NADPH oxidase activity was increased after 2 h of CMS, contributing to the production of O2−. Increased ROS production in lung epithelial cells in response to elevated stretch may contribute to the onset of VILI.

scholarly journals Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

2020 ◽  
Vol 8 ◽  
Author(s):  
Olga Mazuryk ◽  
Grazyna Stochel ◽  
Małgorzata Brindell
Keyword(s):  
Reactive Oxygen Species ◽  
Air Pollution ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Airborne Particulate Matter ◽  
Oxygen Species ◽  
Airborne Particulate ◽  
Inorganic Fraction

Air pollution is associated with numerous negative effects on human health. The toxicity of organic components of air pollution is well-recognized, while the impact of their inorganic counterparts in the overall toxicity is still a matter of various discussions. The influence of airborne particulate matter (PM) and their inorganic components on biological function of human alveolar-like epithelial cells (A549) was investigated in vitro. A novel treatment protocol based on covering culture plates with PM allowed increasing the studied pollutant concentrations and prolonging their incubation time without cell exposure on physical suffocation and mechanical disturbance. PM decreased the viability of A549 cells and disrupted their mitochondrial membrane potential and calcium homeostasis. For the first time, the difference in the reactive oxygen species (ROS) profiles generated by organic and inorganic counterparts of PM was shown. Singlet oxygen generation was observed only after treatment of cells with inorganic fraction of PM, while hydrogen peroxide, hydroxyl radical, and superoxide anion radical were induced after exposure of A549 cells to both PM and their inorganic fraction.

scholarly journals High Glucose Promotes Tumor Invasion and Increases Metastasis-Associated Protein Expression in Human Lung Epithelial Cells by Upregulating Heme Oxygenase-1 via Reactive Oxygen Species or the TGF-β1/PI3K/Akt Signaling Pathway

2015 ◽  
Vol 35 (3) ◽  
pp. 1008-1022 ◽  
Author(s):  
Xiaowen Kang ◽  
Fanwu Kong ◽  
Xiaomei Wu ◽  
Yeping Ren ◽  
Shijie Wu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Human Lung ◽  
Reactive Oxygen ◽  
Lung Epithelial Cells ◽  
Oxygen Species ◽  
Lung Epithelial ◽  
Tgf Β1 ◽  
Human Lung Epithelial Cells

Background: Growing evidence indicates that heme oxygenase-1 (HO-1) is up-regulated in malignancies and subsequently alters tumor aggressiveness and various cancer-related factors, such as high glucose (HG) levels. HO-1 expression can be induced when glucose concentrations are above 25 mM; however, the role of HO-1 in lung cancer patients with diabetes remains unknown. Therefore, in this study we investigated the promotion of tumor cell invasion and the expression of metastasis-associated proteins by inducing the up-regulation of HO-1 expression by HG treatment in A549 human lung epithelial cells. Methods: The expression of HO-1and metastasis-associated protein expression was explored by western blot analysis. HO-1 enzymatic activity, reactive oxygen species (ROS) production and TGF-β1 production were examined by ELISA. Invasiveness was analyzed using a Transwell chamber. Results: HG treatment of A549 cells induced an increase in HO-1 expression, which was mediated by the HG-induced generation of reactive oxygen species (ROS) and transforming growth factor-β1 (TGF-β1) in a concentration- and time-dependent manner. Following the increase in HO-1 expression, the enzymatic activity of HO-1 also increased in HG-treated cells. Pretreatment with N-acetyl-L-cysteine (NAC) or with phosphatidylinositol 3-kinase (PI3K)/Akt inhibitors attenuated the HG-induced increase in HO-1 expression. HG treatment of A549 cells enhanced the invasion potential of these cells, as shown with a Transwell assay, and increased metastasis-associated protein expression. However, HO-1 siRNA transfection significantly decreased these capabilities. Conclusion: this study is the first to demonstrate that HG treatment of A549 human lung epithelial cells promotes tumor cell invasion and increases metastasis-associated protein expression by up-regulating HO-1 expression via ROS or the TGF-β1/PI3K/Akt signaling pathway.

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