Soluble receptor for advanced glycation end-products and progression of airway disease

Iwamoto, Hiroshi; Gao, Jing; Pulkkinen, Ville; Toljamo, Tuula; Nieminen, Pentti; Mazur, Witold

doi:10.1186/1471-2466-14-68

Cited by 57 publications

(58 citation statements)

References 28 publications

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“…Similarly, we did not observe a correlation between decreased lung function and serum or sputum levels of sRAGE ( fig. 1k), as previously reported [14][15][16].…”

supporting

confidence: 58%

“…Therefore, it will be of interest to further elucidate the role of RAGE in exacerbations of COPD. Multiple studies have shown that sRAGE is decreased in serum or plasma of COPD patients, which may act to further potentiate the effect of RAGE ligands [9,[14][15][16]. However, in our study, induced sputum and serum levels of sRAGE did not differ between stable disease and exacerbation (sputum levels 159.5±18.7 and 164.0±21.5 pg·mL −1 , respectively) ( fig.…”

contrasting

confidence: 48%

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Increased serum levels of LL37, HMGB1 and S100A9 during exacerbation in COPD patients

et al. 2015

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Chronic obstructive pulmonary disease (COPD) is a severe and progressive lung disease characterised by destruction of lung parenchyma and chronic airway inflammation [1]. A major cause of COPD is chronic exposure to noxious gases and particles, including cigarette smoke. During exacerbation, COPD patients experience a worsening of symptoms that coincides with increased inflammation and accelerated decline in lung function, resulting in a decrease in quality of life and increased healthcare costs. Approximately half of the COPD exacerbations causing hospitalisation are associated with respiratory viral and/or bacterial infections [2]. However, the underlying mechanisms causing COPD exacerbations are unknown [3]. Molecules derived from viruses and bacteria during airway infection can trigger the activation of pattern recognition receptors (PRRs) on lung structural and innate immune cells, and may thus contribute to the aggravation of inflammation during COPD exacerbations [1]. Interestingly, damage-associated molecular patterns (DAMPs) released from damaged or necrotic cells are also known to activate PRRs, including Toll-like receptors (TLRs) and the receptor for advanced glycation end-products (RAGE) [4]. A role for DAMPs has been proposed in the pathogenesis of COPD, as various DAMPs have been found to be increased in lung fluids and serum of COPD patients [5,6]. Furthermore, Ager, the gene encoding RAGE, has been identified by genome-wide association studies as a susceptibility gene for COPD [7,8]. Moreover, the serum levels of soluble RAGE (sRAGE), a decoy receptor for RAGE, were shown to be significantly lower in COPD patients, while the RAGE ligand EN-RAGE (also known as S100 calcium-binding protein (S100)A12) was significantly higher in COPD patients compared with smoking and nonsmoking controls [9]. It is currently unknown, however, whether DAMPs play a role in COPD exacerbations. Here, we hypothesised that the release of DAMPs is increased during exacerbations of COPD.

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“…Similarly, we did not observe a correlation between decreased lung function and serum or sputum levels of sRAGE ( fig. 1k), as previously reported [14][15][16].…”

supporting

confidence: 58%

contrasting

confidence: 48%

Increased serum levels of LL37, HMGB1 and S100A9 during exacerbation in COPD patients

et al. 2015

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“…The participants were part of a longitudinal study, of a cohort of smokers and nonsmokers, being conducted in northern Finland. The details of the project and the inclusion and exclusion criteria have been previously published (16,20,34,35). In brief, the exclusion criteria consisted of chronic pulmonary or other diseases requiring regular medication, allergies, and risk factors for other pulmonary diseases, e.g., known exposures, bronchiectasis, malignancies, and also previous lung tuberculosis.…”

Section: Methodsmentioning

confidence: 99%

“…In recent proteomic studies from our laboratory the major findings included an elevation of surfactant protein-A (SP-A) and a decrease of specific variants of the receptor for advanced glycation end products (RAGE) in lung tissue (25,26) and polymeric immunoglobulin receptor in sputum samples from patients with COPD (24). Of these, SP-A and soluble RAGE have been validated in longitudinal approaches in larger cohorts (16,20). Our previous proteomics study also identified elevated levels of bactericidal/permeability-increasing protein fold containing protein B1 (BPIFB1, formerly known as LPLUNC1) in induced sputum from smokers and patients with COPD compared with nonsmokers (24).…”

mentioning

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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“…Soluble receptor for advanced glycation end products (sRAGE) consists of the extracellular domain but lacks the trans-membrane and cytoplasmic domains of RAGE in human plasma (9). sRAGE may have an inflammatory or homeostatic role to play in lung tissue (5,10), and is studied as an effective biomarker in ARDS (8,10), ALI (8,10), lung cancer (11) and chronic obstructive pulmonary disease (12).…”

Section: Introductionmentioning

confidence: 99%

The diagnostic utility and tendency of the soluble receptor for advanced glycation end products (sRAGE) in exudative pleural effusion

2016

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Background:The soluble receptor for advanced glycation end products (sRAGE) may have an inflammatory or homeostatic function in lung tissue. The aim of this study was to assess the usefulness of sRAGE as a diagnostic marker for exudative pleural effusions, which are common manifestations of a variety of diseases. Methods:Patients with an undiagnosed pleural effusion were prospectively enrolled between January 2013and January 2015. Samples of blood and pleural fluid were centrifuged and the supernatant stored at −70 °C.The levels of sRAGE in serum and pleural fluid were determined using a commercially available enzymelinked immunosorbent assay (ELISA) kit. Results:In total 47 patients, 21 patients were diagnosed with a tuberculous effusion, and the groups diagnosed with parapneumonic or malignant effusions comprised 13 patients each. The serum sRAGE levels for tuberculosis were significantly elevated [median, 1,291 pg/mL; interquartile range (IQR), 948-1,711 pg/mL] when compared with those for both pneumonia (median, 794 pg/mL; IQR, 700-1,255 pg/mL) and lung cancer (median, 886 pg/mL; IQR, 722-1,285 pg/mL) (P=0.029). The pleural sRAGE levels for pneumonia (median, 1,763 pg/mL; IQR, 1,262-4,431 pg/mL) were lower than those for both tuberculosis (median, 5,081 pg/mL; IQR, 3,300-6,004 pg/mL) and lung cancer (median, 4,936 pg/mL; IQR, 3,282-7,018 pg/mL) (P=0.009) The receiver operating characteristic (ROC) curve analysis selected 896 pg/mL as the best cutoff value in the sRAGE serum level for tuberculosis [sensitivity, 86%; specificity 58%; area under the curve (AUC) =0.727, P=0.008]. For the pleural effusion sRAGE level, the ROC curve analysis selected 2,231 pg/mL as the best cutoff value for pneumonia (sensitivity, 91%; specificity, 62%, AUC =0.792, P=0.002).Conclusions: Among patients with exudative effusion, pleural and serum sRAGE measurements may be useful supportive diagnostic tools in the evaluation of ambiguous pleural effusion. Furthermore, the behavior of sRAGE in the serum and pleural fluid of various pulmonary diseases suggests that sRAGE may be linked to the chronic process of lung damage and inflammation rather than acute bacterial infection.

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Soluble receptor for advanced glycation end-products and progression of airway disease

Cited by 57 publications

References 28 publications

Increased serum levels of LL37, HMGB1 and S100A9 during exacerbation in COPD patients

Increased serum levels of LL37, HMGB1 and S100A9 during exacerbation in COPD patients

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

The diagnostic utility and tendency of the soluble receptor for advanced glycation end products (sRAGE) in exudative pleural effusion

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