Exhaled Nitric Oxide in Chronic Obstructive Pulmonary Disease

Maziak, Wasim; Loukides, Stelios; Culpitt, Sarah V.; Sullivan, Paul; Kharitonov, Sergei A.; Barnes, Peter J.

doi:10.1164/ajrccm.157.3.97-05009

Cited by 282 publications

(211 citation statements)

References 28 publications

(26 reference statements)

Supporting

Mentioning

172

Contrasting

Unclassified

Order By: Relevance

“…Another hypothesis relates smoking-induced pulmonary changes due to COPD as the cause of decreased FeNO in smokers. As stated earlier, while most studies found that FeNO levels increase in patients with COPD [4,45], more recent data from ROY et al [44], using multiple measurements of exhaled NO at different flow rates to model airway NO, suggests that FeNO levels are lower in COPD patients. Like the hypothesis about smokingrelated respiratory epithelial damage, the COPD hypothesis would associate COPD-related inflammatory changes and parenchymal lung damage with reductions in FeNO.…”

Section: Discussionmentioning

confidence: 88%

“…Although ROY et al [44] recently found that COPD was associated with decreased airway NO levels, most studies suggest that COPD is associated with increased FeNO levels [4,45] and, if anything, this would have diminished the difference in FeNO levels between older smokers and nonsmokers. Taken together, the current authors believe that long-term smoking may result in permanent reductions in FeNO levels, possibly via airway epithelial lining changes and changes in NOS2 expression and NO production.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Smoking is associated with an age-related decline in exhaled nitric oxide

Sundy

Hauswirth²,

Mervin-Blake³

et al. 2007

European Respiratory Journal

View full text Add to dashboard Cite

Age-related declines in forced expiratory volume in one second are accelerated in smokers. Smoking is associated with decreased exhaled nitric oxide fraction (FeNO). The aim of the present study was to determine the impact of age on FeNO in otherwise healthy smokers and nonsmokers.FeNO and serum cotinine levels were measured in 994 healthy subjects aged 18-40 yrs. American Thoracic Society questionnaire data on smoking habits was used to validate serum cotinine levels as a surrogate marker for categorisation of smokers and nonsmokers in the cohort.Serum cotinine levels were a good discriminator of smokers (n599) and nonsmokers (n5895). FeNO levels were significantly lower in otherwise healthy smokers compared with nonsmokers. There was an inverse correlation of serum cotinine levels with FeNO. No correlation of age with FeNO was found in nonsmokers but an inverse correlation of FeNO with age in smokers was found. FeNO was significantly lower in smokers aged 21-40 yrs compared with nonsmokers aged 21-40 yrs, but was not lower in smokers aged 18-20 yrs compared with nonsmokers of the same age.Smoking was associated with decreased exhaled nitric oxide. The greatest smoking-related declines in exhaled nitric oxide occurred in older subjects. This suggests that smoking is associated with age-related declines in exhaled nitric oxide and justifies future mechanistic studies that address the impact of exhaled nitric oxide decline on lung function.

show abstract

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Smoking is associated with an age-related decline in exhaled nitric oxide

Sundy

Hauswirth²,

Mervin-Blake³

et al. 2007

European Respiratory Journal

View full text Add to dashboard Cite

show abstract

“…Several investigators [24,25] demonstrated that smoking could reduce endogenous NO production. In this study, there were no significant differences in NO metabolite level in the induced sputum between smokers and nonsmokers in asthmatic subjects as well as in normal controls.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide metabolites in induced sputum: a marker of airway inflammation in asthmatic subjects

Choi²,

et al. 1999

Clin Experimental Allergy

View full text Add to dashboard Cite

SummaryBackground and objective The role of nitric oxide (NO) needs to be further clarified in allergic inflammation. This study was designed to investigate the relationships between NO metabolites and eosinophil count, eosinophil cationic protein (ECP), interleukin (IL)-5 in induced sputum from asthmatics. Methods Hypertonic saline-induced sputum was obtained in 25 asthmatic subjects, among which 13 patients were examined before and after anti-asthmatic medications including steroid preparations. Ten normal subjects were enrolled as controls. Fresh expectorated sputum separated from saliva was treated with equal volume of dithiothreitol 0.1%, cytospined for cell count, and the supernatant was collected for biochemical assay. NO metabolites were assayed by using modified Griess reaction. ECP was measured by fluoroimmunoassay, and detected IL-5 by a sandwich ELISA. Results Asthmatic subjects, compared with controls, had significantly higher concentration of NO metabolites (1035.4 Ϯ 125.3 vs 557.2 Ϯ 101.5 mmol/L, P < 0.01), higher percentage of eosinophils (25.6 Ϯ 4.6 vs 1.7 Ϯ 0.2%, P < 0.01), and higher levels of ECP (1117.8 Ϯ 213.9 vs 154.6 Ϯ 47.4 mg/L, P < 0.01) in the induced sputum. IL-5 was detected more frequently in asthmatic subjects than in control subjects (11/25 [44%] vs 1/10 [10%], P < 0.05). According to asthma severity, moderate to severe asthmatic subjects (n ¼ 18) had higher level of NO metabolites (1143.8 Ϯ 156.3 vs 575.5 Ϯ 89.5 mmol/L, P < 0.01), higher levels of ECP and IL-5 (P < 0.01, respectively) in the induced sputum than in those of mild asthmatic subjects (n ¼ 7). NO metabolites, the percentage of eosinophils, the levels of ECP, and IL-5 were reduced following treatment with anti-asthmatic drugs (P < 0.01, respectively). There were significant positive correlations between NO metabolites and percentage of eosinophils or ECP (r ¼ 0.34, P < 0.05; r ¼ 0.28, P < 0.05). Negative correlations were noted between FEV 1 , FEV 1 /FVC and proportion of eosinophils, ECP, or IL-5 levels. Conclusion These findings confirmed that the level of NO metabolites was increased in the tracheobronchial secretion of asthmatic subjects and was paralleled with severity of asthma. Measurement of NO metabolites in induced sputum may be used for monitoring the degree of airway inflammation in asthmatics.

show abstract

“…Increased exhaled NO levels were observed in ex-smokers with COPD compared to healthy non-smokers, and in current smokers with COPD compared to healthy current smokers (Corradi et al, 1999;Montuschi et al, 2001). Moreover, exhaled NO is increased during COPD exacerbations compared with stable COPD (Maziak et al, 1998). In addition, RNS such as nitrotyrosine and nitrothiol can cause damage to the lung.…”

Section: Ros Rns and Nomentioning

confidence: 96%

The role of oxidative stress in lung injury induced by cigarette smoke

Kluchová

Tkáčová

2006

Biologia

View full text Add to dashboard Cite

Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities -the state of "oxidative stress" -is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

show abstract

Exhaled Nitric Oxide in Chronic Obstructive Pulmonary Disease

Cited by 282 publications

References 28 publications

Smoking is associated with an age-related decline in exhaled nitric oxide

Smoking is associated with an age-related decline in exhaled nitric oxide

Nitric oxide metabolites in induced sputum: a marker of airway inflammation in asthmatic subjects

The role of oxidative stress in lung injury induced by cigarette smoke

Contact Info

Product

Resources

About