Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers
BackgroundInduced sputum is used to sample inflammatory cells, predominantly neutrophils and macrophages, from the airways of COPD patients. The author's aim was to identify candidate genes associated with the degree of airflow obstruction and the extent of emphysema by expression profiling, an...
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| Veröffentlicht in: | Thorax 2011-06, Vol.66 (6), p.489-495 |
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| creator | Singh, Dave Fox, Steven M Tal-Singer, Ruth Plumb, Jonathan Bates, Stewart Broad, Peter Riley, John H Celli, Bartolome |
| description | BackgroundInduced sputum is used to sample inflammatory cells, predominantly neutrophils and macrophages, from the airways of COPD patients. The author's aim was to identify candidate genes associated with the degree of airflow obstruction and the extent of emphysema by expression profiling, and then to confirm these findings for selected candidates using PCR and protein analysis.MethodsTwo sputum studies were performed in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 2–4 COPD ex-smokers from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) cohort. First, gene array profiling at baseline in samples from 148 patients. The findings were replicated in a separate population of 176 patients using real-time PCR. The findings for one selected gene IL-18R were further analysed using immunohistochemistry in lung tissue and induced sputum from patients outside the ECLIPSE cohort.ResultsGene expression profiling revealed changes in 277 genes associated with GOLD stage 2 versus 3 and 4, and 198 genes with changes associated with the degree of emphysema (p |
| doi_str_mv | 10.1136/thx.2010.153767 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_876850472</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4027207911</sourcerecordid><originalsourceid>FETCH-LOGICAL-b430t-f1e34ca72c2f633c82c429227b70f0c5f02f451e0c4c1f3ffa2c4b05ae71c4b73</originalsourceid><addsrcrecordid>eNqFkUtP3DAQgC1UVLbAubfKUoUqIQX8ShyO1bY8JCQ4wNlynDF4SeLFkxT493i1W5C4cPLY8814NB8h3zk74lxWx-P985Fgq1spdaW3yIyrqi6kOKm-kBljihVVTuyQb4gLxljNuf5KdgRXKkdiRuBiaCcHLcXlNE49vYMBkFrE6IId8_tTGO9zMqTYw5iCo3ZoabJtiF28C852tA0IFoEi_IMUxhcaBjq_uv5D4bnAPj5Awj2y7W2HsL85d8nt6d-b-XlxeXV2Mf99WTRKsrHwHKRyVgsnfCWlq4VT4kQI3WjmmSs9E16VHJhTjnvpvc1Aw0oLmudAy13ya913meLjBDiaPqCDrrMDxAlNrau6ZEqLTP78QC7ilIY8nOG65rWoSrmijteUSxExgTfLFHqbXgxnZiXAZAFmJcCsBeSKH5u-U9ND-8b_33gGDjaAxbw9n-zgAr5zSmRpZZm5wzXX9ItPf30FvmSbog</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1781826532</pqid></control><display><type>article</type><title>Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><source>Alma/SFX Local Collection</source><creator>Singh, Dave ; Fox, Steven M ; Tal-Singer, Ruth ; Plumb, Jonathan ; Bates, Stewart ; Broad, Peter ; Riley, John H ; Celli, Bartolome</creator><creatorcontrib>Singh, Dave ; Fox, Steven M ; Tal-Singer, Ruth ; Plumb, Jonathan ; Bates, Stewart ; Broad, Peter ; Riley, John H ; Celli, Bartolome ; ECLIPSE Investigators ; On behalf of the ECLIPSE Investigators</creatorcontrib><description>BackgroundInduced sputum is used to sample inflammatory cells, predominantly neutrophils and macrophages, from the airways of COPD patients. The author's aim was to identify candidate genes associated with the degree of airflow obstruction and the extent of emphysema by expression profiling, and then to confirm these findings for selected candidates using PCR and protein analysis.MethodsTwo sputum studies were performed in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 2–4 COPD ex-smokers from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) cohort. First, gene array profiling at baseline in samples from 148 patients. The findings were replicated in a separate population of 176 patients using real-time PCR. The findings for one selected gene IL-18R were further analysed using immunohistochemistry in lung tissue and induced sputum from patients outside the ECLIPSE cohort.ResultsGene expression profiling revealed changes in 277 genes associated with GOLD stage 2 versus 3 and 4, and 198 genes with changes associated with the degree of emphysema (p<0.01 for each gene). Twelve of these candidate genes were analysed by PCR in the replication cohort, with significant changes (p<0.05) observed for 11 genes. IL-18R protein expression was higher on alveolar macrophages in lung tissue of COPD patients (mean 23.2%) compared to controls (mean ex-smokers 2% and non-smokers 2.5%).ConclusionGene expression profiling in sputum cells identified candidate genes that may play roles in molecular mechanisms associated with COPD. The replication by PCR and protein in different studies confirms these findings, and highlights a potential role for IL-18R upregulation in severe COPD.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thx.2010.153767</identifier><identifier>PMID: 21441172</identifier><identifier>CODEN: THORA7</identifier><language>eng</language><publisher>London: BMJ Publishing Group</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Biosynthesis ; Cardiology. Vascular system ; Cell cycle ; Chronic obstructive pulmonary disease ; Chronic obstructive pulmonary disease, asthma ; Emphysema ; Female ; Gender ; Gene expression ; Gene Expression Profiling - methods ; Humans ; Inflammation ; Longitudinal Studies ; Lung diseases ; Macrophages, Alveolar - metabolism ; Male ; Medical imaging ; Medical sciences ; Metabolism ; Middle Aged ; Neutrophils ; Pathogenesis ; Pneumology ; Polymerase Chain Reaction - methods ; Pulmonary Alveoli - metabolism ; Pulmonary Disease, Chronic Obstructive - diagnostic imaging ; Pulmonary Disease, Chronic Obstructive - genetics ; Pulmonary Disease, Chronic Obstructive - metabolism ; Pulmonary Disease, Chronic Obstructive - physiopathology ; Receptors, Interleukin-18 - genetics ; Receptors, Interleukin-18 - metabolism ; Severity of Illness Index ; Signal transduction ; Smoking ; Smoking Cessation ; Spirometry - methods ; Sputum - cytology ; Sputum - metabolism ; Statistical analysis ; Tomography, X-Ray Computed ; Variance analysis</subject><ispartof>Thorax, 2011-06, Vol.66 (6), p.489-495</ispartof><rights>2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright: 2011 (c) 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b430t-f1e34ca72c2f633c82c429227b70f0c5f02f451e0c4c1f3ffa2c4b05ae71c4b73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://thorax.bmj.com/content/66/6/489.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://thorax.bmj.com/content/66/6/489.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77569,77600</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24204055$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21441172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Singh, Dave</creatorcontrib><creatorcontrib>Fox, Steven M</creatorcontrib><creatorcontrib>Tal-Singer, Ruth</creatorcontrib><creatorcontrib>Plumb, Jonathan</creatorcontrib><creatorcontrib>Bates, Stewart</creatorcontrib><creatorcontrib>Broad, Peter</creatorcontrib><creatorcontrib>Riley, John H</creatorcontrib><creatorcontrib>Celli, Bartolome</creatorcontrib><creatorcontrib>ECLIPSE Investigators</creatorcontrib><creatorcontrib>On behalf of the ECLIPSE Investigators</creatorcontrib><title>Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers</title><title>Thorax</title><addtitle>Thorax</addtitle><description>BackgroundInduced sputum is used to sample inflammatory cells, predominantly neutrophils and macrophages, from the airways of COPD patients. The author's aim was to identify candidate genes associated with the degree of airflow obstruction and the extent of emphysema by expression profiling, and then to confirm these findings for selected candidates using PCR and protein analysis.MethodsTwo sputum studies were performed in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 2–4 COPD ex-smokers from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) cohort. First, gene array profiling at baseline in samples from 148 patients. The findings were replicated in a separate population of 176 patients using real-time PCR. The findings for one selected gene IL-18R were further analysed using immunohistochemistry in lung tissue and induced sputum from patients outside the ECLIPSE cohort.ResultsGene expression profiling revealed changes in 277 genes associated with GOLD stage 2 versus 3 and 4, and 198 genes with changes associated with the degree of emphysema (p<0.01 for each gene). Twelve of these candidate genes were analysed by PCR in the replication cohort, with significant changes (p<0.05) observed for 11 genes. IL-18R protein expression was higher on alveolar macrophages in lung tissue of COPD patients (mean 23.2%) compared to controls (mean ex-smokers 2% and non-smokers 2.5%).ConclusionGene expression profiling in sputum cells identified candidate genes that may play roles in molecular mechanisms associated with COPD. The replication by PCR and protein in different studies confirms these findings, and highlights a potential role for IL-18R upregulation in severe COPD.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Biosynthesis</subject><subject>Cardiology. Vascular system</subject><subject>Cell cycle</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Emphysema</subject><subject>Female</subject><subject>Gender</subject><subject>Gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Longitudinal Studies</subject><subject>Lung diseases</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Neutrophils</subject><subject>Pathogenesis</subject><subject>Pneumology</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Pulmonary Alveoli - metabolism</subject><subject>Pulmonary Disease, Chronic Obstructive - diagnostic imaging</subject><subject>Pulmonary Disease, Chronic Obstructive - genetics</subject><subject>Pulmonary Disease, Chronic Obstructive - metabolism</subject><subject>Pulmonary Disease, Chronic Obstructive - physiopathology</subject><subject>Receptors, Interleukin-18 - genetics</subject><subject>Receptors, Interleukin-18 - metabolism</subject><subject>Severity of Illness Index</subject><subject>Signal transduction</subject><subject>Smoking</subject><subject>Smoking Cessation</subject><subject>Spirometry - methods</subject><subject>Sputum - cytology</subject><subject>Sputum - metabolism</subject><subject>Statistical analysis</subject><subject>Tomography, X-Ray Computed</subject><subject>Variance analysis</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkUtP3DAQgC1UVLbAubfKUoUqIQX8ShyO1bY8JCQ4wNlynDF4SeLFkxT493i1W5C4cPLY8814NB8h3zk74lxWx-P985Fgq1spdaW3yIyrqi6kOKm-kBljihVVTuyQb4gLxljNuf5KdgRXKkdiRuBiaCcHLcXlNE49vYMBkFrE6IId8_tTGO9zMqTYw5iCo3ZoabJtiF28C852tA0IFoEi_IMUxhcaBjq_uv5D4bnAPj5Awj2y7W2HsL85d8nt6d-b-XlxeXV2Mf99WTRKsrHwHKRyVgsnfCWlq4VT4kQI3WjmmSs9E16VHJhTjnvpvc1Aw0oLmudAy13ya913meLjBDiaPqCDrrMDxAlNrau6ZEqLTP78QC7ilIY8nOG65rWoSrmijteUSxExgTfLFHqbXgxnZiXAZAFmJcCsBeSKH5u-U9ND-8b_33gGDjaAxbw9n-zgAr5zSmRpZZm5wzXX9ItPf30FvmSbog</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Singh, Dave</creator><creator>Fox, Steven M</creator><creator>Tal-Singer, Ruth</creator><creator>Plumb, Jonathan</creator><creator>Bates, Stewart</creator><creator>Broad, Peter</creator><creator>Riley, John H</creator><creator>Celli, Bartolome</creator><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</general><scope>IQODW</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110601</creationdate><title>Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers</title><author>Singh, Dave ; Fox, Steven M ; Tal-Singer, Ruth ; Plumb, Jonathan ; Bates, Stewart ; Broad, Peter ; Riley, John H ; Celli, Bartolome</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b430t-f1e34ca72c2f633c82c429227b70f0c5f02f451e0c4c1f3ffa2c4b05ae71c4b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Biosynthesis</topic><topic>Cardiology. Vascular system</topic><topic>Cell cycle</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Emphysema</topic><topic>Female</topic><topic>Gender</topic><topic>Gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Longitudinal Studies</topic><topic>Lung diseases</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Neutrophils</topic><topic>Pathogenesis</topic><topic>Pneumology</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Pulmonary Alveoli - metabolism</topic><topic>Pulmonary Disease, Chronic Obstructive - diagnostic imaging</topic><topic>Pulmonary Disease, Chronic Obstructive - genetics</topic><topic>Pulmonary Disease, Chronic Obstructive - metabolism</topic><topic>Pulmonary Disease, Chronic Obstructive - physiopathology</topic><topic>Receptors, Interleukin-18 - genetics</topic><topic>Receptors, Interleukin-18 - metabolism</topic><topic>Severity of Illness Index</topic><topic>Signal transduction</topic><topic>Smoking</topic><topic>Smoking Cessation</topic><topic>Spirometry - methods</topic><topic>Sputum - cytology</topic><topic>Sputum - metabolism</topic><topic>Statistical analysis</topic><topic>Tomography, X-Ray Computed</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Singh, Dave</creatorcontrib><creatorcontrib>Fox, Steven M</creatorcontrib><creatorcontrib>Tal-Singer, Ruth</creatorcontrib><creatorcontrib>Plumb, Jonathan</creatorcontrib><creatorcontrib>Bates, Stewart</creatorcontrib><creatorcontrib>Broad, Peter</creatorcontrib><creatorcontrib>Riley, John H</creatorcontrib><creatorcontrib>Celli, Bartolome</creatorcontrib><creatorcontrib>ECLIPSE Investigators</creatorcontrib><creatorcontrib>On behalf of the ECLIPSE Investigators</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Singh, Dave</au><au>Fox, Steven M</au><au>Tal-Singer, Ruth</au><au>Plumb, Jonathan</au><au>Bates, Stewart</au><au>Broad, Peter</au><au>Riley, John H</au><au>Celli, Bartolome</au><aucorp>ECLIPSE Investigators</aucorp><aucorp>On behalf of the ECLIPSE Investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>66</volume><issue>6</issue><spage>489</spage><epage>495</epage><pages>489-495</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><coden>THORA7</coden><abstract>BackgroundInduced sputum is used to sample inflammatory cells, predominantly neutrophils and macrophages, from the airways of COPD patients. The author's aim was to identify candidate genes associated with the degree of airflow obstruction and the extent of emphysema by expression profiling, and then to confirm these findings for selected candidates using PCR and protein analysis.MethodsTwo sputum studies were performed in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 2–4 COPD ex-smokers from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) cohort. First, gene array profiling at baseline in samples from 148 patients. The findings were replicated in a separate population of 176 patients using real-time PCR. The findings for one selected gene IL-18R were further analysed using immunohistochemistry in lung tissue and induced sputum from patients outside the ECLIPSE cohort.ResultsGene expression profiling revealed changes in 277 genes associated with GOLD stage 2 versus 3 and 4, and 198 genes with changes associated with the degree of emphysema (p<0.01 for each gene). Twelve of these candidate genes were analysed by PCR in the replication cohort, with significant changes (p<0.05) observed for 11 genes. IL-18R protein expression was higher on alveolar macrophages in lung tissue of COPD patients (mean 23.2%) compared to controls (mean ex-smokers 2% and non-smokers 2.5%).ConclusionGene expression profiling in sputum cells identified candidate genes that may play roles in molecular mechanisms associated with COPD. The replication by PCR and protein in different studies confirms these findings, and highlights a potential role for IL-18R upregulation in severe COPD.</abstract><cop>London</cop><pub>BMJ Publishing Group</pub><pmid>21441172</pmid><doi>10.1136/thx.2010.153767</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Biosynthesis Cardiology. Vascular system Cell cycle Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease, asthma Emphysema Female Gender Gene expression Gene Expression Profiling - methods Humans Inflammation Longitudinal Studies Lung diseases Macrophages, Alveolar - metabolism Male Medical imaging Medical sciences Metabolism Middle Aged Neutrophils Pathogenesis Pneumology Polymerase Chain Reaction - methods Pulmonary Alveoli - metabolism Pulmonary Disease, Chronic Obstructive - diagnostic imaging Pulmonary Disease, Chronic Obstructive - genetics Pulmonary Disease, Chronic Obstructive - metabolism Pulmonary Disease, Chronic Obstructive - physiopathology Receptors, Interleukin-18 - genetics Receptors, Interleukin-18 - metabolism Severity of Illness Index Signal transduction Smoking Smoking Cessation Spirometry - methods Sputum - cytology Sputum - metabolism Statistical analysis Tomography, X-Ray Computed Variance analysis |
| title | Induced sputum genes associated with spirometric and radiological disease severity in COPD ex-smokers |
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