Proteomic study of human bronchoalveolar lavage fluids from smokers with chronic obstructive pulmonary disease by combining surface-enhanced laser desorption/ionization-mass spectrometry profiling with mass spectrometric protein identification

Merkel, Dietrich; Rist, Wolfgang; Seither, Peter; Weith, Andreas; Lenter, Martin

doi:10.1002/pmic.200401180

Cited by 124 publications

(104 citation statements)

References 32 publications

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“…Serum CRP was inversely correlated with both sRAGE levels and FEV1 in the current study, and we recently noted a similar inverse correlation with sRAGE and CRP in rheumatoid arthritis [25]. SAA is also an acute phase protein, but is a known RAGE ligand and can be produced in the lung [32,33]. Our data shows for the first time that plasma SAA is increased in stable COPD relative to healthy subjects.…”

Section: Discussionsupporting

confidence: 55%

Reduced soluble receptor for advanced glycation end-products in COPD

Smith¹,

Yerkovich²,

Towers³

et al. 2010

Eur Respir J

124

100

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The soluble receptor for advanced glycation end-products (sRAGE) has antiinflammatory properties, and deficiency of circulating sRAGE is associated with various human diseases. Whether sRAGE concentrations are reduced in chronic obstructive pulmonary disease (COPD) has not been determined. The aim of this study was to determine plasma levels of sRAGE in COPD patients and establish whether sRAGE varies in relation to forced expiratory volume in 1 s (FEV1) and other inflammatory markers.61 COPD patients and 42 healthy controls were recruited. Plasma sRAGE, C-reactive protein (CRP) and serum amyloid A (SAA) were measured in patients with stable COPD. A subgroup had measurements during acute exacerbations of COPD (AECOPD).sRAGE was significantly lower in stable COPD than in healthy controls (p,0.001), while CRP (p,0.001) and SAA (p50.015) were higher in stable COPD than in healthy controls. Multiple linear regression confirmed that COPD was negatively associated with sRAGE (p,0.001). Plasma sRAGE was positively correlated with FEV1 (r 2 50.530, p,0.001), while CRP and SAA were inversely proportional to FEV1. Multiple linear regression analysis showed that only sRAGE was a strong predictor of FEV1. AECOPD were associated with even lower sRAGE levels that increased with convalescence. Circulating sRAGE is lower in COPD and shows a strong correlation to the degree of airflow limitation.

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Section: Discussionsupporting

confidence: 55%

Reduced soluble receptor for advanced glycation end-products in COPD

Smith¹,

Yerkovich²,

Towers³

et al. 2010

Eur Respir J

124

100

View full text Add to dashboard Cite

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“…S100s or myeloid-related proteins are a family of calciumbinding proteins that are expressed in the cytosol of neutrophils, monocytes and macrophages. S100A9 concentration in BAL fluid is increased in COPD patients compared with asymptomatic smokers, as is S100A8 concentration in the BAL fluid of asymptomatic smokers versus nonsmokers [190]. S100A8/14 have been shown to be endogenous factors in lung secretions that can stimulate IL-8 production by airway epithelial cells [191].…”

Section: Lung Cytokines/chemokinesmentioning

confidence: 99%

Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction

Chung¹,

Adcock²

2008

Eur Respir J

517

425

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Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair.Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response.An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases.The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.

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“…Along with ADH7, these are crucial enzymes in retinoic acid metabolism, a hormone known as important regulator of organ development and homeostasis, including lung [37]. To what COPD is concerned, we also identified in nasal epithelial cells three proteins reported to be differentially expressed in BALF of COPD patients -Neutrophil defensins 1 and calgranulin A and B - [38]. In sputum, the clara cell secretory protein (CCSP) was also reported as potential COPD biomarker [39].…”

mentioning

confidence: 80%

Proteomics in Detection and Monitoring Chronic Lung Diseases: The Human Nasal Epithelium as a Molecular Model

Simões¹

2012

J Aller Ther

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Allergy & Therapy Simões et al., J Aller Ther 2012, S7 http://dx.doi.org/10.4172/2155Asthma and chronic obstructive pulmonary disease (COPD) are major causes of mortality and morbidity worldwide. The current state-of-art diagnosis and management schemes are suboptimal for both diseases as the incidence of asthma has risen by 250% over the last two decades and COPD is estimated to become the third leading cause of death worldwide within the next decade. Additionally, these diseases represent a very important threat to global economies in direct and indirect medical costs and lost working days [1,2]. Asthma is a chronic inflammatory disorder of the airways associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung [1]. Chronic airflow obstruction is also characteristic of COPD but, in contrast to asthma, is not fully reversible, even under the action of bronchodilators, and is usually progressive. A combination of small airway disease -obstructive bronchiolitis -and parenchymal destruction -emphysema, leads to COPD clinical manifestation [2]. A number of factors influence a person's risk of developing these lung diseases, which include host factors, primarily genetic, and environmental factors, such as allergens and tobacco smoke in asthma and COPD, respectively [1][2][3].

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Proteomic study of human bronchoalveolar lavage fluids from smokers with chronic obstructive pulmonary disease by combining surface-enhanced laser desorption/ionization-mass spectrometry profiling with mass spectrometric protein identification

Cited by 124 publications

References 32 publications

Reduced soluble receptor for advanced glycation end-products in COPD

Reduced soluble receptor for advanced glycation end-products in COPD

Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction

Proteomics in Detection and Monitoring Chronic Lung Diseases: The Human Nasal Epithelium as a Molecular Model

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