Effect of Ozone Exposure on Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

Todokoro, Makoto; Mochizuki, Hiroyuki; Tokuyama, Kenichi; Utsugi, Mitsuyoshi; Dobashi, Kunio; Mori, Masatomo; Morikawa, Akihiro

doi:10.1023/b:ifla.0000033026.91221.ed

Cited by 21 publications

(24 citation statements)

References 38 publications

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“…At 6-12 h after A549 cells and NHBE cells were exposed to RSV, the intracellular redox state changed to a severely oxidized state, followed by a prolonged reduced state. Airway epithelial cells have an effective mechanism to improve an oxidized state, particularly the glutathione redox system, which can rapidly return cells from an oxidized to a reduced state [26]. Although previous studies have demonstrated an association between RSV infection and oxidative stress [31,32], this is the first study that documents the time-dependent effect of RSV infection on the intracellular redox state and proved that RSV induce oxidative stress in cultured human airway epithelial cells.…”

Section: Discussionmentioning

confidence: 76%

“…The current results suggest that RSV infection up-regulated IL-8 and other cytokine/chemokine production by means of oxidative stress in A549 cells and NHBE cells. In a previous study, oxidative stress affected the signal transfer system in airway epithelial cells resulting in up-regulation of cytokine/chemokine production, especially of IL-8 [26].…”

Section: Discussionmentioning

confidence: 90%

“…Previous studies have shown that RSV infection activates NF-κB and IRF-3 pathways [26,47,48], and both are central mediators of antiviral cytokine expression. Either oxidants or oxidative stress have been reported to activate transcription factors including NF-κB [49,50].…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress-induced intracellular redox changes occur in a time-dependent manner [26]. We used RSV with 1×10 5 PFU/ml in this study.…”

Section: Rsv Infection and Intracellular Redox State In A549mentioning

confidence: 99%

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RS Virus-Induced Inflammation and the Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

2009

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There is ample evidence that asthma is mediated by oxidative stress and that viral infection, which is associated with asthma onset and exacerbation in infants, acts as one type of oxidative stress. The goal of this study was to determine whether respiratory syncytial virus (RSV) induces oxidative stress in cultured A549 human airway epithelial cells and normal human bronchial epithelial cells (NHBE), and whether such RSV-induced oxidative stress can induce airway inflammation. To evaluate the direct effect of RSV infection as an oxidative stressor, the intracellular levels of reduced glutathione (GSH) or oxidized glutathione (GSSG) were measured. Their ratio (GSH/GSSG) was calculated to indicate intracellular oxidation-reduction (redox) status in A549 and NHBE. To evaluate the extent to which glutathione redox regulation affected cytokine/chemokine production, the effect of pretreatment with a reductive agent, glutathione monoethyl ester (GSH-OEt) and RSV-specific monoclonal antibody was thus studied. RSV acted as a potent oxidative stressor on the intracellular glutathione redox state in human airway epithelial cells, activating signals to increase the production of cytokine/chemokine. Pretreatment with GSH-OEt significantly suppressed RSV-induced time-dependent changes in the intracellular redox state, and also suppressed RSV-induced up-regulation of epithelial cell-derived IL-8, IL-6 and eotaxin production, as well as RSV-specific monoclonal antibody. RSV-induced oxidative stress is likely to contribute to the perpetuation and amplification of the inflammatory response. Therapeutic intervention against oxidative stress might therefore be beneficial as adjunctive therapies for respiratory disorders that are caused by an RSV infection.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress-induced intracellular redox changes occur in a time-dependent manner [26]. We used RSV with 1×10 5 PFU/ml in this study.…”

Section: Rsv Infection and Intracellular Redox State In A549mentioning

confidence: 99%

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RS Virus-Induced Inflammation and the Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

2009

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“…This result could be due to the sampling time point, since it has been shown to a reliable biomarker in nasal lavage fluid (Keman et al 1998;Sienra-Monge et al 2004). In the in vitro study of Todokoro et al (2004), it was observed that the IL-8 production started to increase after the second hour post-exposure, and only after 6 h did the upregulation of this cytokine become apparent. Therefore, we possibly missed this time point.…”

Section: Discussionmentioning

confidence: 99%

Impact of heat and pollution on oxidative stress and CC16 secretion after 8 km run

2011

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To investigate the acute effect of a hot, humid and ozone-polluted (O(3)) environment on lung inflammation and oxidative tress of runners performing 8 km time trial run. Using a single-blinded randomized design, 10 male athletes (mean[Formula: see text]= 64.4 mlO(2) kg(-1) min(-1), SD = 4.4) took part in a time trial run in four different environmental conditions: 20°C + 50% relative humidity (rh) (Control); 20°C + 50% rh + 0.10 ppm O(3) (Control + O(3)); 31°C + 70% rh (Heat); 31°C + 70% rh + 0.10 ppm O(3) (Heat + O(3)). Blood samples and nasal lavage were collected post-exercise and analyzed for inflammatory, epithelial damage and oxidative stress markers. Data were analyzed using repeated measures ANOVA with Tukey's post hoc test. A significant increase in CC16 concentration (P < 0.05) and GSH/protein concentration (P < 0.05) in the upper respiratory airways was observed following the 8 km run in the Heat + O(3) trial compared with the control trial. There were no differences in the neutrophil counts between trials. No differences were observed for the other antioxidants analyzed. A hot, humid and ozone-polluted environment (0.1 ppm) elicits an early epithelial damage and antioxidant protection process in the upper respiratory airways of athletes immediately after performing 8 km time trial run.

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Impact of ozone exposure on prostaglandin release in nasal polyps

Zhu

Fruth

Schneider

et al. 2011

Eur Arch Otorhinolaryngol

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A dysregulation of the cyclooxygenases and a leukotriene/prostaglandin imbalance are assumed to be part of the pathogenesis of the aspirin (ASA) intolerance syndrome. Ozone is an air pollutant with known proinflammatory effects on exposed epithelia, however, its impact on the expression of the cyclooxygenases 1 and 2 (cox1/2) and prostaglandin E(2) (PGE(2)) in the nasal mucosa is not well known. Therefore, we analyzed cox expression and PGE(2) levels after ozone exposure in nasal mucosa and in nasal polyps considering ASA intolerance. Isolated epithelial nasal cells from control subjects without chronic rhinosinusitis (CRS), and those from patients with nasal polyps with and without ASA intolerance were cultured and exposed in vitro to ozone. Cox1/2 expression levels were analyzed by immunohistochemistry and PGE(2) release by ELISA. After ozone exposure cox1/2 expression remained unchanged in all the three groups. PGE(2) release was lowered in cell cultures from controls and from polyps of ASA tolerant but not in those of ASA intolerant patients after ozone exposure. In the latter, PGE(2) expression remained unchanged. Our in vitro data suggest that aspirin tolerant patients with polyps might be more affected by ozone compared to aspirin intolerant ones. The potential clinical impact of impaired PGE(2) expression caused by ozone on the functions of respiratory epithelia remains to be clarified.

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Effect of Ozone Exposure on Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

Cited by 21 publications

References 38 publications

RS Virus-Induced Inflammation and the Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

RS Virus-Induced Inflammation and the Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

Impact of heat and pollution on oxidative stress and CC16 secretion after 8 km run

Impact of ozone exposure on prostaglandin release in nasal polyps

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