Increased oxidative stress in asymptomatic current chronic smokers and GOLD stage 0 COPD

Rytilä, Paula; Rehn, Tiina; Ilumets, Helen; Rouhos, Annamari; Sovijärvi, Anssi; Myllärniemi, Marjukka; Kinnula, Vuokko L.

doi:10.1186/1465-9921-7-69

Cited by 69 publications

(77 citation statements)

References 44 publications

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“…Two years later, smoking status was assessed and baseline BD spirometry, plasma and sputum samples were collected during 2007-2008 (16, 20, 35). Sputum was processed by using the sputum plug method as described (27,31). Only represen- Characteristics of participants in the lung tissue sample studies.…”

Section: Methodsmentioning

confidence: 99%

Elevated sputum BPIFB1 levels in smokers with chronic obstructive pulmonary disease: a longitudinal study

Gao

Ohlmeier

Nieminen

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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-A previous study involving a proteomic screen of induced sputum from smokers and patients with chronic obstructive pulmonary disease (COPD) demonstrated elevated levels of bactericidal/permeability-increasing foldcontaining protein B1 (BPIFB1). The aim of the present study was to further evaluate the association of sputum BPIFB1 levels with smoking and longitudinal changes in lung function in smokers with COPD. Sputum BPIFB1 was characterized by two-dimensional gel electrophoresis and mass spectrometry. The expression of BPIFB1 in COPD was investigated by immunoblotting and immunohistochemistry using sputum and lung tissue samples. BPIFB1 levels were also assessed in induced sputum from nonsmokers (n ϭ 31), smokers (n ϭ 169), and patients with COPD (n ϭ 52) via an ELISA-based method. The longitudinal changes in lung function during the 4-year follow-up period were compared with the baseline sputum BPIFB1 levels. In lung tissue samples, BPIFB1 was localized to regions of goblet cell metaplasia. Secreted and glycosylated BPIFB1 was significantly elevated in the sputum of patients with COPD compared with that of smokers and nonsmokers. Sputum BPIFB1 levels correlated with pack-years and lung function as measured by forced expiratory volume in 1 s (FEV 1) % predicted and FEV1/FVC (forced vital capacity) at baseline and after the 4-year follow-up in all participants. The changes in lung function over 4 years were significantly associated with BPIFB1 levels in current smokers with COPD. In conclusion, higher sputum concentrations of BPIFB1 were associated with changes of lung function over time, especially in current smokers with COPD. BPIFB1 may be involved in the pathogenesis of smokingrelated lung diseases.

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Section: Methodsmentioning

confidence: 99%

Elevated sputum BPIFB1 levels in smokers with chronic obstructive pulmonary disease: a longitudinal study

Gao

Ohlmeier

Nieminen

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Sputum was induced, as described by the European Respiratory Society Task Force, with 4.5% physiological saline solution [21], and samples processed as previously described [22]. Briefly, expectorated samples were processed with four volumes of dithioerythritol (DTE; Sigma, Munich, Germany).…”

Section: Sputum Processingmentioning

confidence: 99%

8-Isoprostane as a marker of oxidative stress in nonsymptomatic cigarette smokers and COPD

Kinnula¹,

Ilumets²,

Myllärniemi³

et al. 2006

Eur Respir J

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8-Isoprostane is a potential in vivo marker for oxidant burden, but its usefulness in induced sputum of smokers and chronic obstructive pulmonary disease (COPD) has not been investigated.The current study investigated 58 subjects comprising 11 never-smokers, 11 ex-smokers, 13 healthy current smokers and 23 COPD with stage 0-III disease (according to the Global Initiative for Chronic Obstructive Lung Disease criteria). 8-Isoprostane was determined from induced sputum by enzyme immunoassay.Sputum 8-isoprostane levels were similar in the never-smokers and ex-smokers, but were elevated in the healthy smokers compared with nonsmokers, and in those with stage I-III COPD. Sputum 8-isoprostane levels could not differentiate nonsymptomatic smokers from those with Stage 0 COPD. There was a correlation between sputum 8-isoprostane level and lung function parameters (forced expiratory volume in one second/forced vital capacity and sputum neutrophils.In conclusion, sputum 8-isoprostane levels correlate with the severity of chronic obstructive pulmonary disease. However, they do not appear to differentiate healthy smokers from those who are at risk of developing chronic obstructive pulmonary disease (Global Initiative for Chronic Obstructive Lung Disease stage 0). KEYWORDS: Chronic obstructive pulmonary disease, cigarette smoking, oxidant, sputum C hronic obstructive pulmonary disease (COPD) is generally diagnosed when lung function parameters have become significantly reduced and a major part of the lung has been damaged. The pathogenesis of COPD has been strongly associated with reactive oxygen species [1-4], although it is not known how oxidative/nitrosative stress predicts the disease progression. Several oxidant markers and ''footprints'' of oxidative/nitrosative damage have been detected in COPD lung tissue, sputum, exhaled air and exhaled breath condensate [3][4][5][6], but it has not been unequivocally resolved whether these biomarkers can be used in the early assessment of cigarette-smoke-related lung diseases, their progression or whether they relate to smoking alone.8-Epi-prostaglandinF 2a (8-isoprostane) has been suggested to be the most reliable approach to monitor oxidative stress in vivo [7,8]. Isoprostanes are formed by free-radical-catalysed lipid peroxidation of arachidonic acid and cell membrane phospholipids. Isoprostanes can also be released into the circulation, secretions and urine where levels have been found to be stable and reproducible in many experimental approaches [8,9]. Isoprostanes also have potent biological actions and therefore they may significantly contribute to the progression of oxidant-mediated lung diseases, such as COPD.Several studies have shown elevated 8-isoprostane in the exhaled breath condensate of COPD patients [10][11][12][13]. There are, however, a number of uncertainties with respect to the usefulness and standardisation of exhaled breath condensate [14][15][16][17]. One recent study also failed to detect 8-isoprostane in exhaled breath condensate in the majority o...

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“…The resulting tissue damage that occurs as a result of oxidative stress can help drive an inflammatory response (2). In chronic obstructive pulmonary disease (COPD), oxidative stress due to cigarette smoke is considered to be the main etiologic factor in disease pathogenesis (3,4). The disease is characterized by a chronic inflammatory response, leading to a progressive and poorly reversible airflow limitation (5) that is resistant to corticosteroid therapy (6,7).…”

mentioning

confidence: 99%

Curcumin Restores Corticosteroid Function in Monocytes Exposed to Oxidants by Maintaining HDAC2

Meja¹,

Saravanan²,

Adenuga³

et al. 2008

Am J Respir Cell Mol Biol

182

109

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Oxidative stress as a result of cigarette smoking is an important etiologic factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic steroid-insensitive inflammatory disease of the airways. Histone deacetylase-2 (HDAC2), a critical component of the corticosteroid anti-inflammatory action, is impaired in lungs of patients with COPD and correlates with disease severity. We demonstrate here that curcumin (diferuloylmethane), a dietary polyphenol, at nanomolar concentrations specifically restores cigarette smoke extract (CSE)-or oxidative stress-impaired HDAC2 activity and corticosteroid efficacy in vitro with an EC 50 of approximately 30 nM and 200 nM, respectively. CSE caused a reduction in HDAC2 protein expression that was restored by curcumin. This decrease in HDAC2 protein expression was reversed by curcumin even in the presence of cycloheximide, a protein synthesis inhibitor. The proteasomal inhibitor, MG132, also blocked CSE-induced HDAC2 degradation, increasing the levels of ubiquitinated HDAC2. Biochemical and gene chip analysis indicated that curcumin at concentrations up to 1 mM propagates its effect via antioxidant-independent mechanisms associated with the phosphorylation-ubiquitin-proteasome pathway. Thus curcumin acts at a post-translational level by maintaining both HDAC2 activity and expression, thereby reversing steroid insensitivity induced by either CSE or oxidative stress in monocytes. Curcumin may therefore have potential to reverse steroid resistance, which is common in patients with COPD and asthma.

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Increased oxidative stress in asymptomatic current chronic smokers and GOLD stage 0 COPD

Abstract: Our results clearly indicate that several markers of oxidative/nitrosative stress are increased in current cigarette smokers compared to non-smokers and no major differences can be observed in these biomarkers between non-symptomatic smokers and subjects with GOLD stage 0 COPD.

Cited by 69 publications

References 44 publications

Elevated sputum BPIFB1 levels in smokers with chronic obstructive pulmonary disease: a longitudinal study

Elevated sputum BPIFB1 levels in smokers with chronic obstructive pulmonary disease: a longitudinal study

8-Isoprostane as a marker of oxidative stress in nonsymptomatic cigarette smokers and COPD

Curcumin Restores Corticosteroid Function in Monocytes Exposed to Oxidants by Maintaining HDAC2

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