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Cited by 389Chronic Obstructive Pulmonary Disease (COPD) ResearchAsthma and respiratory diseasesCystic Fibrosis Research Advances

Oxidative stress and airway inflammation in severe exacerbations of COPD

Open access
Drost, E M·2005·Thorax
DOI 10.1136/thx.2004.027946PMC PMC1747355
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Abstract

BACKGROUND: A study was undertaken to assess both oxidative stress and inflammation in the lungs of patients with chronic obstructive pulmonary disease (COPD) during severe and very severe exacerbations compared with those with stable COPD, healthy smokers, and non-smokers. Two sites within the lungs were compared: the large airways (in sputum) and the peripheral airways (by bronchoalveolar lavage (BAL)). METHODS: BAL fluid cell numbers and levels of tumour necrosis factor (TNFalpha) and interleukin (IL)-8 were measured as markers of airway inflammation and glutathione (GSH) levels as a marker of antioxidant status. Nuclear translocation of the pro-inflammatory transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein 1 (AP-1) were also measured by electromobility shift assay in BAL fluid leucocytes and lung biopsy samples. RESULTS: Influx of inflammatory cells into the peripheral airways during exacerbations of COPD was confirmed. Increased IL-8 levels were detected in BAL fluid from patients with stable COPD compared with non-smokers and healthy smokers, with no further increase during exacerbations. In contrast, IL-8 levels in the large airways increased during exacerbations. GSH levels were increased in the BAL fluid of smokers (444%) and patients with stable COPD (235%) compared with non-smokers and were reduced during exacerbations (severe 89.2%; very severe 52.3% compared with stable COPD). NF-kappaB DNA binding in BAL leucocytes was decreased in healthy smokers compared with non-smokers (41.3%, n = 9, p<0.001) but did not differ in COPD patients, whereas AP-1 DNA binding was significantly decreased during exacerbations of COPD. CONCLUSION: There is evidence of increased oxidative stress in the airways of patients with COPD that is increased further in severe and very severe exacerbations of the disease. This is associated with increased neutrophil influx and IL-8 levels during exacerbations.

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  • Exogenous sources including tobacco smoke, asbestos, radon, and others increase ROS formation, which activates transcription factors NF-κB and AP-1.

    “Exogenous sources, involving tobacco smoke, asbestos, radon, and others increase ROS formation which consequently activates transcription factors NF-κB and activator protein AP-1.”

    From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Drost et al. 2005

  • These transcription factors are responsible for gene transcription of proinflammatory cytokines such as TNF-α and interleukins IL-8 and IL-6, which sequestrate leukocytes such as neutrophils and macrophages, forming part of an inflammatory pathway.

    “These transcription factors are responsible for the gene transcription of proinflammatory cytokines, such as tumor necrosis factor (TNF-α) and interleukins IL-8 and IL-6 which in turn sequestrate leukocytes such as neutrophils and macrophages forming thus a part of an inflammatory pathway (Drost et al. 2005; Federico et al. 2007).”

    From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Drost et al. 2005

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  1. Drost EM, Ritchie HE, Skwarska E, et al. NF-kB activation in airway leucocytes in COPD patients. Eur Respir J 2001;16:260s.

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Authors
Drost, E. M.
Affiliations
Centre for Inflammation Research (GB)
Corresponding author
Drost, E M
Venue
Thorax
Publisher
BMJ
Published
2005-04-01
Volume
60
Issue
4
Pages
293-300
ISSN
0040-6376 (ISSN-L)
DOI
10.1136/thx.2004.027946
PMC
PMC1747355
OpenAlex
W2108983987
Cited by
389
References
51
Citations by year
2026: 5 · 2025: 10 · 2024: 9 · 2023: 23 · 2022: 26 · 2021: 18 · 2020: 19 · 2019: 6 · 2018: 15 · 2017: 20 · 2016: 9 · 2015: 15 · 2014: 30 · 2013: 25 · 2012: 15
FWCI
19.98
Type
journal article
Language
en
Open access
Locations
  • Thorax (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cystic Fibrosis Research Advances
Keywords
chronic obstructive pulmonary disease, COPD exacerbations, oxidative stress, airway inflammation, bronchoalveolar lavage, sputum, glutathione, antioxidant status, TNF-α, interleukin-8, neutrophil influx, NF-κB, AP-1, transcription factor-DNA binding, smokers
MeSH terms
Bronchitis, Bronchoalveolar Lavage Fluid, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Middle Aged, Tumor Necrosis Factor-alpha, Interleukin-8, NF-kappa B, Oxidative Stress, Electrophoretic Mobility Shift Assay, Pulmonary Disease, Chronic Obstructive

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