Airway Angiogenesis in Stable and Exacerbated Chronic Obstructive Pulmonary Disease

Angiogenesis is a prominent feature of structural tissue remodelling that occurs in chronic airway diseases, including chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the airway levels of VEGF, angiogenin, IL‐8 and TNF‐α in patients with COPD during the stable pha...

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Veröffentlicht in:Scandinavian journal of immunology 2012-01, Vol.75 (1), p.109-114
Hauptverfasser: Kristan, S. S., Marc, M. M., Kern, I., Flezar, M., Suskovic, S., Kosnik, M., Korosec, P.
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container_end_page 114
container_issue 1
container_start_page 109
container_title Scandinavian journal of immunology
container_volume 75
creator Kristan, S. S.
Marc, M. M.
Kern, I.
Flezar, M.
Suskovic, S.
Kosnik, M.
Korosec, P.
description Angiogenesis is a prominent feature of structural tissue remodelling that occurs in chronic airway diseases, including chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the airway levels of VEGF, angiogenin, IL‐8 and TNF‐α in patients with COPD during the stable phase and during acute exacerbation of the disease. We analysed induced sputum samples from 28 patients with COPD. Thirteen of these patients were followed up and second samples of sputum were obtained during acute exacerbation of the disease. The two control groups consisted of 12 healthy smokers and seven healthy non‐smokers, all with normal lung function tests. Concentrations of VEGF, angiogenin, IL‐8, TNF‐α and bFGF were measured by cytometric bead array. In the induced sputum of patients with stable COPD, concentrations of VEGF (P 
doi_str_mv 10.1111/j.1365-3083.2011.02623.x
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S. ; Marc, M. M. ; Kern, I. ; Flezar, M. ; Suskovic, S. ; Kosnik, M. ; Korosec, P.</creator><creatorcontrib>Kristan, S. S. ; Marc, M. M. ; Kern, I. ; Flezar, M. ; Suskovic, S. ; Kosnik, M. ; Korosec, P.</creatorcontrib><description><![CDATA[Angiogenesis is a prominent feature of structural tissue remodelling that occurs in chronic airway diseases, including chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the airway levels of VEGF, angiogenin, IL‐8 and TNF‐α in patients with COPD during the stable phase and during acute exacerbation of the disease. We analysed induced sputum samples from 28 patients with COPD. Thirteen of these patients were followed up and second samples of sputum were obtained during acute exacerbation of the disease. The two control groups consisted of 12 healthy smokers and seven healthy non‐smokers, all with normal lung function tests. Concentrations of VEGF, angiogenin, IL‐8, TNF‐α and bFGF were measured by cytometric bead array. In the induced sputum of patients with stable COPD, concentrations of VEGF (P < 0.001, P = 0.02), angiogenin (P < 0.0001, P < 0.0001), IL‐8 (P < 0.0001, P = 0.0021) and TNF‐α (P < 0.001, P = 0.03) were significantly elevated in comparison with healthy smokers and non‐smokers. No additional elevation of angiogenic factors was demonstrated at the time of exacerbation. There was a significant negative correlation between FEV1 and VEGF (P < 0.05, r = −0.38), angiogenin (P < 0.0001, r = −0.68) and IL‐8 (P < 0.001, r = −0.54) among smokers (smoking COPD patients and healthy smokers). No significant differences were observed between groups of healthy smokers and non‐smokers. These results showed increased airway angiogenesis in patients with COPD. Moreover, VEGF, IL‐8 and angiogenin negatively correlated with pulmonary function, which suggests their important role in COPD airway remodelling. However, no additional angiogenic activation was found during exacerbation of COPD.]]></description><identifier>ISSN: 0300-9475</identifier><identifier>EISSN: 1365-3083</identifier><identifier>DOI: 10.1111/j.1365-3083.2011.02623.x</identifier><identifier>PMID: 21916917</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Aged ; Angiogenesis ; Angiogenin ; Chronic obstructive pulmonary disease ; Female ; Fibroblast growth factor 2 ; Fibroblast Growth Factor 2 - metabolism ; Flow Cytometry ; Humans ; Interleukin 8 ; Interleukin-8 - metabolism ; Lung - blood supply ; Male ; Middle Aged ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - pathology ; Pulmonary Disease, Chronic Obstructive - metabolism ; Pulmonary Disease, Chronic Obstructive - pathology ; Respiratory Function Tests ; Respiratory tract diseases ; Ribonuclease, Pancreatic - metabolism ; Smoking ; Sputum ; Sputum - metabolism ; Statistics, Nonparametric ; Tumor necrosis factor- alpha ; Tumor Necrosis Factor-alpha - metabolism ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism ; Young Adult</subject><ispartof>Scandinavian journal of immunology, 2012-01, Vol.75 (1), p.109-114</ispartof><rights>2011 The Authors. 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S.</creatorcontrib><creatorcontrib>Marc, M. M.</creatorcontrib><creatorcontrib>Kern, I.</creatorcontrib><creatorcontrib>Flezar, M.</creatorcontrib><creatorcontrib>Suskovic, S.</creatorcontrib><creatorcontrib>Kosnik, M.</creatorcontrib><creatorcontrib>Korosec, P.</creatorcontrib><title>Airway Angiogenesis in Stable and Exacerbated Chronic Obstructive Pulmonary Disease</title><title>Scandinavian journal of immunology</title><addtitle>Scand J Immunol</addtitle><description><![CDATA[Angiogenesis is a prominent feature of structural tissue remodelling that occurs in chronic airway diseases, including chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the airway levels of VEGF, angiogenin, IL‐8 and TNF‐α in patients with COPD during the stable phase and during acute exacerbation of the disease. We analysed induced sputum samples from 28 patients with COPD. Thirteen of these patients were followed up and second samples of sputum were obtained during acute exacerbation of the disease. The two control groups consisted of 12 healthy smokers and seven healthy non‐smokers, all with normal lung function tests. Concentrations of VEGF, angiogenin, IL‐8, TNF‐α and bFGF were measured by cytometric bead array. In the induced sputum of patients with stable COPD, concentrations of VEGF (P < 0.001, P = 0.02), angiogenin (P < 0.0001, P < 0.0001), IL‐8 (P < 0.0001, P = 0.0021) and TNF‐α (P < 0.001, P = 0.03) were significantly elevated in comparison with healthy smokers and non‐smokers. No additional elevation of angiogenic factors was demonstrated at the time of exacerbation. There was a significant negative correlation between FEV1 and VEGF (P < 0.05, r = −0.38), angiogenin (P < 0.0001, r = −0.68) and IL‐8 (P < 0.001, r = −0.54) among smokers (smoking COPD patients and healthy smokers). No significant differences were observed between groups of healthy smokers and non‐smokers. These results showed increased airway angiogenesis in patients with COPD. Moreover, VEGF, IL‐8 and angiogenin negatively correlated with pulmonary function, which suggests their important role in COPD airway remodelling. However, no additional angiogenic activation was found during exacerbation of COPD.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Angiogenesis</subject><subject>Angiogenin</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Female</subject><subject>Fibroblast growth factor 2</subject><subject>Fibroblast Growth Factor 2 - metabolism</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Interleukin 8</subject><subject>Interleukin-8 - metabolism</subject><subject>Lung - blood supply</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Pulmonary Disease, Chronic Obstructive - metabolism</subject><subject>Pulmonary Disease, Chronic Obstructive - pathology</subject><subject>Respiratory Function Tests</subject><subject>Respiratory tract diseases</subject><subject>Ribonuclease, Pancreatic - metabolism</subject><subject>Smoking</subject><subject>Sputum</subject><subject>Sputum - metabolism</subject><subject>Statistics, Nonparametric</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Young Adult</subject><issn>0300-9475</issn><issn>1365-3083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtu2zAQRYmgQeIk_YWCu66k8C1pkYXh5lU4D8BtsyRIapTQlSWXlBr77yPVqbctN0Ngzh1yDkKYkpQO53yZUq5kwknOU0YoTQlTjKebAzTZNz6gCeGEJIXI5DE6iXFJCOUs40fomNGCqoJmE7SY-vBqtnjaPPv2GRqIPmLf4EVnbA3YNCW-3BgHwZoOSjx7CW3jHX6wsQu96_xvwI99vWobE7b4i49gIpyhw8rUET6-11P0_ery2-wmmT9c386m88RJKXiijKyMlAXNuakcr5S1ShIBQrCSlUpmxFaFMZIoJqQFp0oqhuVELpwh1uT8FH3ezV2H9lcPsdMrHx3UtWmg7aMuGMmKXEjyb5LSQrDhIwOZ70gX2hgDVHod_GpYTlOiR_d6qUfFelSsR_f6j3u9GaKf3h_p7QrKffCv7AG42AGvvobtfw_Wi6-3423IJ7u8jx1s9nkTfmqV8Uzqp_trPb-6E-Tux5Pm_A36AqDy</recordid><startdate>201201</startdate><enddate>201201</enddate><creator>Kristan, S. S.</creator><creator>Marc, M. M.</creator><creator>Kern, I.</creator><creator>Flezar, M.</creator><creator>Suskovic, S.</creator><creator>Kosnik, M.</creator><creator>Korosec, P.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201201</creationdate><title>Airway Angiogenesis in Stable and Exacerbated Chronic Obstructive Pulmonary Disease</title><author>Kristan, S. S. ; Marc, M. 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S.</creatorcontrib><creatorcontrib>Marc, M. M.</creatorcontrib><creatorcontrib>Kern, I.</creatorcontrib><creatorcontrib>Flezar, M.</creatorcontrib><creatorcontrib>Suskovic, S.</creatorcontrib><creatorcontrib>Kosnik, M.</creatorcontrib><creatorcontrib>Korosec, P.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Scandinavian journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kristan, S. S.</au><au>Marc, M. 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Thirteen of these patients were followed up and second samples of sputum were obtained during acute exacerbation of the disease. The two control groups consisted of 12 healthy smokers and seven healthy non‐smokers, all with normal lung function tests. Concentrations of VEGF, angiogenin, IL‐8, TNF‐α and bFGF were measured by cytometric bead array. In the induced sputum of patients with stable COPD, concentrations of VEGF (P < 0.001, P = 0.02), angiogenin (P < 0.0001, P < 0.0001), IL‐8 (P < 0.0001, P = 0.0021) and TNF‐α (P < 0.001, P = 0.03) were significantly elevated in comparison with healthy smokers and non‐smokers. No additional elevation of angiogenic factors was demonstrated at the time of exacerbation. There was a significant negative correlation between FEV1 and VEGF (P < 0.05, r = −0.38), angiogenin (P < 0.0001, r = −0.68) and IL‐8 (P < 0.001, r = −0.54) among smokers (smoking COPD patients and healthy smokers). No significant differences were observed between groups of healthy smokers and non‐smokers. These results showed increased airway angiogenesis in patients with COPD. Moreover, VEGF, IL‐8 and angiogenin negatively correlated with pulmonary function, which suggests their important role in COPD airway remodelling. However, no additional angiogenic activation was found during exacerbation of COPD.]]></abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21916917</pmid><doi>10.1111/j.1365-3083.2011.02623.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Angiogenesis
Angiogenin
Chronic obstructive pulmonary disease
Female
Fibroblast growth factor 2
Fibroblast Growth Factor 2 - metabolism
Flow Cytometry
Humans
Interleukin 8
Interleukin-8 - metabolism
Lung - blood supply
Male
Middle Aged
Neovascularization, Pathologic - metabolism
Neovascularization, Pathologic - pathology
Pulmonary Disease, Chronic Obstructive - metabolism
Pulmonary Disease, Chronic Obstructive - pathology
Respiratory Function Tests
Respiratory tract diseases
Ribonuclease, Pancreatic - metabolism
Smoking
Sputum
Sputum - metabolism
Statistics, Nonparametric
Tumor necrosis factor- alpha
Tumor Necrosis Factor-alpha - metabolism
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - metabolism
Young Adult
title Airway Angiogenesis in Stable and Exacerbated Chronic Obstructive Pulmonary Disease
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