The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease
The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothes...
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| Veröffentlicht in: | PloS one 2011-09, Vol.6 (9), p.e24399-e24399 |
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| creator | Hector, Andreas Kormann, Michael S D Mack, Ines Latzin, Philipp Casaulta, Carmen Kieninger, Elisabeth Zhou, Zhe Yildirim, Ali Ö Bohla, Alexander Rieber, Nikolaus Kappler, Matthias Koller, Barbara Eber, Ernst Eickmeier, Olaf Zielen, Stefan Eickelberg, Oliver Griese, Matthias Mall, Marcus A Hartl, Dominik |
| description | The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothesized that YKL-40 plays a key role in cystic fibrosis (CF) lung disease, a prototypic neutrophilic disease. The aim of this study was (i) to analyze YKL-40 levels in human and murine CF lung disease and (ii) to investigate whether YKL-40 single-nucleotide polymorphisms (SNPs) modulate CF lung disease severity. YKL-40 protein levels were quantified in serum and sputum supernatants from CF patients and control individuals. Levels of the murine homologue BRP-39 were analyzed in airway fluids from CF-like βENaC-Tg mice. YKL-40SNPs were analyzed in CF patients. YKL-40 levels were increased in sputum supernatants and in serum from CF patients compared to healthy control individuals. Within CF patients, YKL-40 levels were higher in sputum than in serum. BRP-39 levels were increased in airways fluids from βENaC-Tg mice compared to wild-type littermates. In both CF patients and βENaC-Tg mice, YKL-40/BRP-39 airway levels correlated with the severity of pulmonary obstruction. Two YKL-40 SNPs (rs871799 and rs880633) were found to modulate age-adjusted lung function in CF patients. YKL-40/BRP-39 levelsare increased in human and murine CF airway fluids, correlate with pulmonary function and modulate CF lung disease severity genetically. These findings suggest YKL-40 as a potential biomarker in CF lung disease. |
| doi_str_mv | 10.1371/journal.pone.0024399 |
| format | Article |
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Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothesized that YKL-40 plays a key role in cystic fibrosis (CF) lung disease, a prototypic neutrophilic disease. The aim of this study was (i) to analyze YKL-40 levels in human and murine CF lung disease and (ii) to investigate whether YKL-40 single-nucleotide polymorphisms (SNPs) modulate CF lung disease severity. YKL-40 protein levels were quantified in serum and sputum supernatants from CF patients and control individuals. Levels of the murine homologue BRP-39 were analyzed in airway fluids from CF-like βENaC-Tg mice. YKL-40SNPs were analyzed in CF patients. YKL-40 levels were increased in sputum supernatants and in serum from CF patients compared to healthy control individuals. Within CF patients, YKL-40 levels were higher in sputum than in serum. BRP-39 levels were increased in airways fluids from βENaC-Tg mice compared to wild-type littermates. In both CF patients and βENaC-Tg mice, YKL-40/BRP-39 airway levels correlated with the severity of pulmonary obstruction. Two YKL-40 SNPs (rs871799 and rs880633) were found to modulate age-adjusted lung function in CF patients. YKL-40/BRP-39 levelsare increased in human and murine CF airway fluids, correlate with pulmonary function and modulate CF lung disease severity genetically. These findings suggest YKL-40 as a potential biomarker in CF lung disease.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0024399</identifier><identifier>PMID: 21949714</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipokines - blood ; Adipokines - genetics ; Adipokines - metabolism ; Allergies ; Analysis ; Animals ; Apoptosis ; Asthma ; Biology ; Biomarkers ; Children & youth ; Chitinase ; Chitinase-3-Like Protein 1 ; Chronic obstructive pulmonary disease ; Cystic fibrosis ; Cystic Fibrosis - genetics ; Cystic Fibrosis - metabolism ; Cystic Fibrosis - pathology ; Female ; Fluids ; Genes ; Genetic aspects ; Homology ; Hospitals ; Humans ; Inflammation ; Lectins - blood ; Lectins - genetics ; Lectins - metabolism ; Leukocytes (neutrophilic) ; Lung cancer ; Lung diseases ; Male ; Medical research ; Mice ; Mutation ; Neutrophils ; Obstructive lung disease ; Patients ; Pediatrics ; Polymorphism, Single Nucleotide ; Proteins ; Pulmonary functions ; Respiratory diseases ; Respiratory function ; Respiratory tract ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Sputum ; Sputum - metabolism ; Type 2 diabetes ; Young Adult</subject><ispartof>PloS one, 2011-09, Vol.6 (9), p.e24399-e24399</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Hector et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Hector et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-bcaf7e1352dde5b529edb0c77fe56a8cc5389a69f104393d6eee27056aad87473</citedby><cites>FETCH-LOGICAL-c691t-bcaf7e1352dde5b529edb0c77fe56a8cc5389a69f104393d6eee27056aad87473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176766/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176766/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21949714$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hector, Andreas</creatorcontrib><creatorcontrib>Kormann, Michael S D</creatorcontrib><creatorcontrib>Mack, Ines</creatorcontrib><creatorcontrib>Latzin, Philipp</creatorcontrib><creatorcontrib>Casaulta, Carmen</creatorcontrib><creatorcontrib>Kieninger, Elisabeth</creatorcontrib><creatorcontrib>Zhou, Zhe</creatorcontrib><creatorcontrib>Yildirim, Ali Ö</creatorcontrib><creatorcontrib>Bohla, Alexander</creatorcontrib><creatorcontrib>Rieber, Nikolaus</creatorcontrib><creatorcontrib>Kappler, Matthias</creatorcontrib><creatorcontrib>Koller, Barbara</creatorcontrib><creatorcontrib>Eber, Ernst</creatorcontrib><creatorcontrib>Eickmeier, Olaf</creatorcontrib><creatorcontrib>Zielen, Stefan</creatorcontrib><creatorcontrib>Eickelberg, Oliver</creatorcontrib><creatorcontrib>Griese, Matthias</creatorcontrib><creatorcontrib>Mall, Marcus A</creatorcontrib><creatorcontrib>Hartl, Dominik</creatorcontrib><title>The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothesized that YKL-40 plays a key role in cystic fibrosis (CF) lung disease, a prototypic neutrophilic disease. The aim of this study was (i) to analyze YKL-40 levels in human and murine CF lung disease and (ii) to investigate whether YKL-40 single-nucleotide polymorphisms (SNPs) modulate CF lung disease severity. YKL-40 protein levels were quantified in serum and sputum supernatants from CF patients and control individuals. Levels of the murine homologue BRP-39 were analyzed in airway fluids from CF-like βENaC-Tg mice. YKL-40SNPs were analyzed in CF patients. YKL-40 levels were increased in sputum supernatants and in serum from CF patients compared to healthy control individuals. Within CF patients, YKL-40 levels were higher in sputum than in serum. BRP-39 levels were increased in airways fluids from βENaC-Tg mice compared to wild-type littermates. In both CF patients and βENaC-Tg mice, YKL-40/BRP-39 airway levels correlated with the severity of pulmonary obstruction. Two YKL-40 SNPs (rs871799 and rs880633) were found to modulate age-adjusted lung function in CF patients. YKL-40/BRP-39 levelsare increased in human and murine CF airway fluids, correlate with pulmonary function and modulate CF lung disease severity genetically. These findings suggest YKL-40 as a potential biomarker in CF lung disease.</description><subject>Adipokines - blood</subject><subject>Adipokines - genetics</subject><subject>Adipokines - metabolism</subject><subject>Allergies</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Asthma</subject><subject>Biology</subject><subject>Biomarkers</subject><subject>Children & youth</subject><subject>Chitinase</subject><subject>Chitinase-3-Like Protein 1</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cystic fibrosis</subject><subject>Cystic Fibrosis - genetics</subject><subject>Cystic Fibrosis - metabolism</subject><subject>Cystic Fibrosis - pathology</subject><subject>Female</subject><subject>Fluids</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Homology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lectins - blood</subject><subject>Lectins - genetics</subject><subject>Lectins - metabolism</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mutation</subject><subject>Neutrophils</subject><subject>Obstructive lung disease</subject><subject>Patients</subject><subject>Pediatrics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proteins</subject><subject>Pulmonary functions</subject><subject>Respiratory diseases</subject><subject>Respiratory function</subject><subject>Respiratory tract</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Sputum</subject><subject>Sputum - metabolism</subject><subject>Type 2 diabetes</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNklGL1DAUhYso7jr6D0QLguJDx6Rpk-ZFWBZ1BwcWdBV8Cml622ZMm9kmFfffmzrdZSr7YPPQkHznJPfmRNFzjNaYMPxuZ8ehl2a9tz2sEUozwvmD6BRzkiY0ReTh0fwkeuLcDqGcFJQ-jk5SzDPOcHYaXVy1EKtWe91LB4nRPyHeD9aD7uMfn7dJhuLOVqORHlysbpzXKq51OVinXWzGvokr7SBIn0aPamkcPJv_q-jbxw9X5xfJ9vLT5vxsmyjKsU9KJWsGmORpVUFe5imHqkSKsRpyKgulwhW5pLzGKBREKgoAKUNhT1YFyxhZRS8PvntjnZib4AQmqMgRJXkRiM2BqKzcif2gOzncCCu1-Ltgh0bIIdRhQHCW1RyTEqRMM8YID30peclTxrAi4VtF7-fTxrKDSkHvB2kWpsudXreisb8EwYwySoPBm9lgsNcjOC867RQYI3uwoxMFzwpMUTEV9uof8v7iZqqR4f66r204Vk2e4ixjtGAF4pPX-h4qjAo6rUJgah3WF4K3C0FgPPz2jRydE5uvX_6fvfy-ZF8fsS1I41tnzei17d0SzA6gCtFyA9R3PcZITHm_7YaY8i7mvAfZi-P3uRPdBpz8AYit-Y8</recordid><startdate>20110920</startdate><enddate>20110920</enddate><creator>Hector, Andreas</creator><creator>Kormann, Michael S D</creator><creator>Mack, Ines</creator><creator>Latzin, Philipp</creator><creator>Casaulta, Carmen</creator><creator>Kieninger, Elisabeth</creator><creator>Zhou, Zhe</creator><creator>Yildirim, Ali Ö</creator><creator>Bohla, Alexander</creator><creator>Rieber, Nikolaus</creator><creator>Kappler, Matthias</creator><creator>Koller, Barbara</creator><creator>Eber, Ernst</creator><creator>Eickmeier, Olaf</creator><creator>Zielen, Stefan</creator><creator>Eickelberg, Oliver</creator><creator>Griese, Matthias</creator><creator>Mall, Marcus A</creator><creator>Hartl, Dominik</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110920</creationdate><title>The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease</title><author>Hector, Andreas ; Kormann, Michael S D ; Mack, Ines ; Latzin, Philipp ; Casaulta, Carmen ; Kieninger, Elisabeth ; Zhou, Zhe ; Yildirim, Ali Ö ; Bohla, Alexander ; Rieber, Nikolaus ; Kappler, Matthias ; Koller, Barbara ; Eber, Ernst ; Eickmeier, Olaf ; Zielen, Stefan ; Eickelberg, Oliver ; Griese, Matthias ; Mall, Marcus A ; Hartl, Dominik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-bcaf7e1352dde5b529edb0c77fe56a8cc5389a69f104393d6eee27056aad87473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adipokines - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content 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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hector, Andreas</au><au>Kormann, Michael S D</au><au>Mack, Ines</au><au>Latzin, Philipp</au><au>Casaulta, Carmen</au><au>Kieninger, Elisabeth</au><au>Zhou, Zhe</au><au>Yildirim, Ali Ö</au><au>Bohla, Alexander</au><au>Rieber, Nikolaus</au><au>Kappler, Matthias</au><au>Koller, Barbara</au><au>Eber, Ernst</au><au>Eickmeier, Olaf</au><au>Zielen, Stefan</au><au>Eickelberg, Oliver</au><au>Griese, Matthias</au><au>Mall, Marcus A</au><au>Hartl, Dominik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-09-20</date><risdate>2011</risdate><volume>6</volume><issue>9</issue><spage>e24399</spage><epage>e24399</epage><pages>e24399-e24399</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothesized that YKL-40 plays a key role in cystic fibrosis (CF) lung disease, a prototypic neutrophilic disease. The aim of this study was (i) to analyze YKL-40 levels in human and murine CF lung disease and (ii) to investigate whether YKL-40 single-nucleotide polymorphisms (SNPs) modulate CF lung disease severity. YKL-40 protein levels were quantified in serum and sputum supernatants from CF patients and control individuals. Levels of the murine homologue BRP-39 were analyzed in airway fluids from CF-like βENaC-Tg mice. YKL-40SNPs were analyzed in CF patients. YKL-40 levels were increased in sputum supernatants and in serum from CF patients compared to healthy control individuals. Within CF patients, YKL-40 levels were higher in sputum than in serum. BRP-39 levels were increased in airways fluids from βENaC-Tg mice compared to wild-type littermates. In both CF patients and βENaC-Tg mice, YKL-40/BRP-39 airway levels correlated with the severity of pulmonary obstruction. Two YKL-40 SNPs (rs871799 and rs880633) were found to modulate age-adjusted lung function in CF patients. YKL-40/BRP-39 levelsare increased in human and murine CF airway fluids, correlate with pulmonary function and modulate CF lung disease severity genetically. These findings suggest YKL-40 as a potential biomarker in CF lung disease.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21949714</pmid><doi>10.1371/journal.pone.0024399</doi><tpages>e24399</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-09, Vol.6 (9), p.e24399-e24399 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1308506358 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adipokines - blood Adipokines - genetics Adipokines - metabolism Allergies Analysis Animals Apoptosis Asthma Biology Biomarkers Children & youth Chitinase Chitinase-3-Like Protein 1 Chronic obstructive pulmonary disease Cystic fibrosis Cystic Fibrosis - genetics Cystic Fibrosis - metabolism Cystic Fibrosis - pathology Female Fluids Genes Genetic aspects Homology Hospitals Humans Inflammation Lectins - blood Lectins - genetics Lectins - metabolism Leukocytes (neutrophilic) Lung cancer Lung diseases Male Medical research Mice Mutation Neutrophils Obstructive lung disease Patients Pediatrics Polymorphism, Single Nucleotide Proteins Pulmonary functions Respiratory diseases Respiratory function Respiratory tract Single nucleotide polymorphisms Single-nucleotide polymorphism Sputum Sputum - metabolism Type 2 diabetes Young Adult |
| title | The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease |
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