Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients

Oxidative stress in the lung is important in the pathogenesis of COPD. Published data indicate that glucocorticoids inhibit blood cells in their capacity to produce reactive oxygen species (ROS). We investigated the effect of Fluticasone propionate (FP) on the ROS production capabilities of pulmonar...

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Main Authors: Gert T. Verhoeven, Annemarie J.M. Wijkhuijs, Herbert Hooijkaas, Henk C. Hoogsteden, Wim Sluiter
Format: Article
Language:English
Published: Wiley 2000-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1080/096293500411578
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author Gert T. Verhoeven
Annemarie J.M. Wijkhuijs
Herbert Hooijkaas
Henk C. Hoogsteden
Wim Sluiter
author_facet Gert T. Verhoeven
Annemarie J.M. Wijkhuijs
Herbert Hooijkaas
Henk C. Hoogsteden
Wim Sluiter
author_sort Gert T. Verhoeven
collection DOAJ
description Oxidative stress in the lung is important in the pathogenesis of COPD. Published data indicate that glucocorticoids inhibit blood cells in their capacity to produce reactive oxygen species (ROS). We investigated the effect of Fluticasone propionate (FP) on the ROS production capabilities of pulmonary cells. Bronchoalveolar lavage (BAL) was performed in smoking COPD patients, before and after a six month, placebo-controlled treatment with FP. BAL cells were stimulated with phorbol myristrate acetate (PMA) alone, and together with superoxide dismutase (SOD). From kinetic plots of ferricytochrome-c conversion we calculated the maximal rate of superoxide production: Vmax. We also examined BAL cell subsets and performed correlation analyses on ROS production and relevant clinical determinants. Paired results were obtained from 6 FP- and 9 placebo-treated patients. No significant change of Vmax was found in both patient groups. Also BAL cellularity was unchanged. Correlation analyses showed a significant (inverse) association of Vmax with the number of cigarettes smoked per day. We concluded that a potent inhaled glucocorticoid had no effect on the ROS production capability of BAL cells from smoking COPD patients. Apparently, heavy smoking impaired the ability of alveolar macrophages to produce ROS, which was not further decreased by FP.
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spelling doaj-art-920d7cd9d0394453b53cc5af8f3490342025-02-03T05:51:59ZengWileyMediators of Inflammation0962-93511466-18612000-01-019210911310.1080/096293500411578Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patientsGert T. Verhoeven0Annemarie J.M. Wijkhuijs1Herbert Hooijkaas2Henk C. Hoogsteden3Wim Sluiter4Department of Pulmonary and Intensive Care Medicine, Erasmus University Medical Center Rotterdam, The NetherlandsDepartment of Immunology, Erasmus University Medical Center Rotterdam, The NetherlandsDepartment of Immunology, Erasmus University Medical Center Rotterdam, The NetherlandsDepartment of Pulmonary and Intensive Care Medicine, Erasmus University Medical Center Rotterdam, The NetherlandsDepartment of Biochemistry, Erasmus University Medical Center Rotterdam, The NetherlandsOxidative stress in the lung is important in the pathogenesis of COPD. Published data indicate that glucocorticoids inhibit blood cells in their capacity to produce reactive oxygen species (ROS). We investigated the effect of Fluticasone propionate (FP) on the ROS production capabilities of pulmonary cells. Bronchoalveolar lavage (BAL) was performed in smoking COPD patients, before and after a six month, placebo-controlled treatment with FP. BAL cells were stimulated with phorbol myristrate acetate (PMA) alone, and together with superoxide dismutase (SOD). From kinetic plots of ferricytochrome-c conversion we calculated the maximal rate of superoxide production: Vmax. We also examined BAL cell subsets and performed correlation analyses on ROS production and relevant clinical determinants. Paired results were obtained from 6 FP- and 9 placebo-treated patients. No significant change of Vmax was found in both patient groups. Also BAL cellularity was unchanged. Correlation analyses showed a significant (inverse) association of Vmax with the number of cigarettes smoked per day. We concluded that a potent inhaled glucocorticoid had no effect on the ROS production capability of BAL cells from smoking COPD patients. Apparently, heavy smoking impaired the ability of alveolar macrophages to produce ROS, which was not further decreased by FP.http://dx.doi.org/10.1080/096293500411578
spellingShingle Gert T. Verhoeven
Annemarie J.M. Wijkhuijs
Herbert Hooijkaas
Henk C. Hoogsteden
Wim Sluiter
Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
Mediators of Inflammation
title Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
title_full Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
title_fullStr Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
title_full_unstemmed Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
title_short Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients
title_sort effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking copd patients
url http://dx.doi.org/10.1080/096293500411578
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