Oxidant-induced corticosteroid unresponsiveness in human bronchial epithelial cells

Heijink, Irene H.; Oosterhout, Antoon van; Kliphuis, Nathalie M.; Jonker, Marnix; Hoffmann, Roland; Telenga, Eef D.; Klooster, Karin; Slebos, Dirk‐Jan; Hacken, Nick ten; Postma, Dirkje S.; Berge, Maarten van den

doi:10.1136/thoraxjnl-2013-203520

Cited by 63 publications

(55 citation statements)

References 35 publications

(38 reference statements)

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“…show that 16HBE cells stimulated with H2O2, cytomix and LPS upregulated IL-8 mRNA expression, in agreement with previously reported observations [30][31][32][33][34][35][36][37]. This was associated with upregulation of p38α MAPK but not JNK1 and ERK1 mRNA after H2O2 and LPS exposure.…”

Section: Discussionsupporting

confidence: 81%

“…Wnt-4-stimulated 16HBE cells significantly increased IL-8 secretion and p38 MAPK activation [35]. A lower efficacy of corticosteroids is reported in human bronchial epithelial cells in asthma and COPD after oxidative stress challenge [2,36]. In paediatric bronchial epithelial cells, Th2 cytokine challenge in the presence of rhinovirus-16 infection augmented IL-8 release [29].…”

Section: Discussionmentioning

confidence: 99%

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Phospho-p38 MAPK Expression in COPD Patients and Asthmatics and in Challenged Bronchial Epithelium

et al. 2015

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Phospho-p38 MAPK Expression in COPD Patients and Asthmatics and in Challenged Bronchial Epithelium

et al. 2015

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“…The findings here have major implications to the respiratory physiology. Cell junctions represent an essential part of the barrier to the outside world formed by airway epithelial cells, and disruption of these junctions or loss of junctional proteins has been found in asthma and cystic fibrosis patients (Georas and Rezaee 2014; Heijink et al 2014; Rezaee and Georas 2014). As another key observation, enhanced airway angiogenesis has also been associated with asthma (Ribatti et al 2009) and cystic fibrosis (Verhaeghe et al 2007).…”

Section: Discussionmentioning

confidence: 99%

The impact of oil spill to lung health—Insights from an RNA-seq study of human airway epithelial cells

Liu

Roy-Engel

Baddoo

et al. 2016

Gene

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The Deepwater Horizon oil spill (BP oil spill) in the Gulf of Mexico was a unique disaster event, where a huge amount of oil spilled from the sea bed and a large volume of dispersants were applied to clean the spill. The operation lasted for almost three months and involved >50,000 workers. The potential health hazards to these workers may be significant as previous research suggested an association of persistent respiratory symptoms with exposure to oil and oil dispersants. To reveal the potential effects of oil and oil dispersants on the respiratory system at the molecular level, we evaluated the transcriptomic profile of human airway epithelial cells grown under treatment of crude oil, the dispersants Corexit 9500 and Corexit 9527 and oil-dispersant mixtures. We identified a very strong effect of Corexit 9500 treatment, with 84 genes (response genes) differentially expressed in treatment vs. control samples. We discovered an interactive effect of oil-dispersant mixtures; while no response gene was found for Corexit 9527 treatment alone, cells treated with Corexit 9527 + oil mixture showed an increased number of response genes (46 response genes), suggesting a synergic effect of 9527 with oil on airway epithelial cells. Through GO (gene ontology) functional term and pathway-based analysis, we identified upregulation of gene sets involved in angiogenesis and immune responses and downregulation of § Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript gene sets involved in cell junctions and steroid synthesis as the prevailing transcriptomic signatures in the cells treated with Corexit 9500, oil or Corexit 9500 + oil mixture. Interestingly, these key molecular signatures coincide with important pathological features observed in common lung diseases, such as asthma, cystic fibrosis and chronic obstructive pulmonary disease. Our study provides mechanistic insights into the detrimental effects of oil and oil dispersants to the respiratory system and suggests significant health impacts of the recent BP oil spill to those people involved in the cleaning operation.

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“…Moreover, dexamethasone can directly induce oxidative stress in osteoblasts and hippocampal cells (30). As far as other glucocorticoids are concerned, although fluticasone and budesonide showed protective effects on H 2 O 2 -induced inflammation in alveolar macrophages in a previous study (27), budesonide could not protect 16HBE cells from H 2 O 2 -induced oxidative stress (31), and budesonide had no effects on H 2 O 2 production in vitro (32). Treatment with fluticasone also has no effects on the concentrations of expired H 2 O 2 in patients (33).…”

Section: Discussionmentioning

confidence: 99%

Procaterol but Not Dexamethasone Protects 16HBE Cells From H2O2-Induced Oxidative Stress

et al. 2014

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Abstract.Oxidative stress is an important pathophysiological factor of asthma and chronic obstructive pulmonary disease (COPD). We hypothesized that procaterol and dexamethasone might treat inflammation through inhibiting oxidative stress in vitro. This study evaluated procaterol and dexamethasone in the hydrogen peroxide (H 2 O 2 )-induced immortal human bronchial epithelial cell model of oxidative stress and investigated the underlying mechanisms. Results showed that exposure to 125 mM H 2 O 2 for 2 h led to a 50% reduction in the cell viability, significantly increased the percentage of apoptosis, and elevated levels of malondialdehyde and reactive oxygen species. Pretreatment with procaterol (25 -200 nM) could reduce these effects in a dosedependent manner. In contrast, pretreatment with dexamethasone (100 nM, 1000 nM) was inefficient. Pretreatment with procaterol plus dexamethasone (100 nM procaterol + 1000 nM dexamethasone) was effective, but the combined effect was not more effective than the sole pretreatment with 100 nM procaterol. The nuclear factor kappa-B (NF-kB) pathway was involved in the pathogenic mechanisms of H 2 O 2 . Procaterol may indirectly inhibit H 2 O 2 -induced activation of the NF-kB pathway due to its capability of antioxidation. Glucocorticoids may be not recommended to treat asthma or COPD complicated with severe oxidative stress.

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Oxidant-induced corticosteroid unresponsiveness in human bronchial epithelial cells

Cited by 63 publications

References 35 publications

Phospho-p38 MAPK Expression in COPD Patients and Asthmatics and in Challenged Bronchial Epithelium

Phospho-p38 MAPK Expression in COPD Patients and Asthmatics and in Challenged Bronchial Epithelium

The impact of oil spill to lung health—Insights from an RNA-seq study of human airway epithelial cells

Procaterol but Not Dexamethasone Protects 16HBE Cells From H2O2-Induced Oxidative Stress

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