Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis
Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology. The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts a...
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| creator | Buendía-Roldán, Ivette Ruiz, Víctor Sierra, Patricia Montes, Eduardo Ramírez, Remedios Vega, Anita Salgado, Alfonso Vargas, Mario H Mejía, Mayra Pardo, Annie Selman, Moisés |
| description | Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology. The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts and finally the excessive accumulation of extracellular matrix with the consequent destruction of the lung parenchyma. CC16 (approved symbol SCGB1A1), a putative anti-inflammatory protein produced by "club" cells in the distal airways, has not been evaluated in IPF lungs. In this study, we determined the serum and bronchoalveolar lavage (BAL) levels as well as the lung cell localization of this protein. Also, we explored the usefulness of serum levels of CC16 for the differential diagnosis of IPF (n = 85), compared with non-IPF interstitial lung diseases [chronic hypersensitivity pneumonitis (cHP; n = 85) and connective tissue diseases (CTD-ILD; n = 85)]. CC16 was significantly increased in serum and BAL fluids of IPF patients and was found not only in club cells but also in alveolar epithelial cells. When compared with non-IPF patients and controls, serum levels were significantly increased (p |
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The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts and finally the excessive accumulation of extracellular matrix with the consequent destruction of the lung parenchyma. CC16 (approved symbol SCGB1A1), a putative anti-inflammatory protein produced by "club" cells in the distal airways, has not been evaluated in IPF lungs. In this study, we determined the serum and bronchoalveolar lavage (BAL) levels as well as the lung cell localization of this protein. Also, we explored the usefulness of serum levels of CC16 for the differential diagnosis of IPF (n = 85), compared with non-IPF interstitial lung diseases [chronic hypersensitivity pneumonitis (cHP; n = 85) and connective tissue diseases (CTD-ILD; n = 85)]. CC16 was significantly increased in serum and BAL fluids of IPF patients and was found not only in club cells but also in alveolar epithelial cells. When compared with non-IPF patients and controls, serum levels were significantly increased (p<0.0001). Sensitivity and specificity for CC16 (cut-off 41ng/mL) were 24% and 90%, positive predictive value 56% and negative predictive value 69%. These findings demonstrate that CC16 is upregulated in IPF patients suggesting that may participate in its pathogenesis. Although higher than the serum levels of non-IPF patients it shows modest sensitivity to be useful as a potential biomarker for the differential diagnosis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0168552</identifier><identifier>PMID: 27977812</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aberration ; Aged ; Alveoli ; Alveolitis ; Bioindicators ; Biology and Life Sciences ; Biomarkers ; Biomarkers - blood ; Biomarkers - metabolism ; Bronchi - cytology ; Bronchi - metabolism ; Bronchoalveolar lavage ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchus ; Cell migration ; Cell proliferation ; Cellular proteins ; Chronic obstructive pulmonary disease ; Connective tissue diseases ; Connective tissues ; Development and progression ; Diagnosis ; Differential diagnosis ; Epithelial cells ; Epithelial Cells - metabolism ; Etiology ; Extracellular matrix ; Family medical history ; Female ; Fibroblasts ; Fibrosis ; Gene expression ; Genetic aspects ; Humans ; Hypersensitivity ; Idiopathic Pulmonary Fibrosis - blood ; Idiopathic Pulmonary Fibrosis - diagnosis ; Idiopathic Pulmonary Fibrosis - metabolism ; Inflammation ; Localization ; Lung diseases ; Lung Diseases, Interstitial - blood ; Lung Diseases, Interstitial - diagnosis ; Lung Diseases, Interstitial - metabolism ; Lungs ; Male ; Medical diagnosis ; Medicine and Health Sciences ; Middle Aged ; Parenchyma ; Pathogenesis ; Patients ; People and Places ; Physiological aspects ; Pneumonia ; Pneumonitis ; Population ; Proteins ; Pulmonary Alveoli - cytology ; Pulmonary Alveoli - metabolism ; Pulmonary fibrosis ; Research and Analysis Methods ; Rheumatoid arthritis ; Rheumatology ; Rodents ; Sensitivity ; Serum levels ; Sex Factors ; Tomography ; Uteroglobin - blood ; Uteroglobin - metabolism</subject><ispartof>PloS one, 2016-12, Vol.11 (12), p.e0168552-e0168552</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Buendía-Roldán et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://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>2016 Buendía-Roldán et al 2016 Buendía-Roldán et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-b093b3006e6e21b469ddae601e73fd8c2fb63a4764bc4c878f71d6b565aa63523</citedby><cites>FETCH-LOGICAL-c725t-b093b3006e6e21b469ddae601e73fd8c2fb63a4764bc4c878f71d6b565aa63523</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/PMC5158056/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5158056/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27977812$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Morty, Rory Edward</contributor><creatorcontrib>Buendía-Roldán, Ivette</creatorcontrib><creatorcontrib>Ruiz, Víctor</creatorcontrib><creatorcontrib>Sierra, Patricia</creatorcontrib><creatorcontrib>Montes, Eduardo</creatorcontrib><creatorcontrib>Ramírez, Remedios</creatorcontrib><creatorcontrib>Vega, Anita</creatorcontrib><creatorcontrib>Salgado, Alfonso</creatorcontrib><creatorcontrib>Vargas, Mario H</creatorcontrib><creatorcontrib>Mejía, Mayra</creatorcontrib><creatorcontrib>Pardo, Annie</creatorcontrib><creatorcontrib>Selman, Moisés</creatorcontrib><title>Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology. The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts and finally the excessive accumulation of extracellular matrix with the consequent destruction of the lung parenchyma. CC16 (approved symbol SCGB1A1), a putative anti-inflammatory protein produced by "club" cells in the distal airways, has not been evaluated in IPF lungs. In this study, we determined the serum and bronchoalveolar lavage (BAL) levels as well as the lung cell localization of this protein. Also, we explored the usefulness of serum levels of CC16 for the differential diagnosis of IPF (n = 85), compared with non-IPF interstitial lung diseases [chronic hypersensitivity pneumonitis (cHP; n = 85) and connective tissue diseases (CTD-ILD; n = 85)]. CC16 was significantly increased in serum and BAL fluids of IPF patients and was found not only in club cells but also in alveolar epithelial cells. When compared with non-IPF patients and controls, serum levels were significantly increased (p<0.0001). Sensitivity and specificity for CC16 (cut-off 41ng/mL) were 24% and 90%, positive predictive value 56% and negative predictive value 69%. These findings demonstrate that CC16 is upregulated in IPF patients suggesting that may participate in its pathogenesis. Although higher than the serum levels of non-IPF patients it shows modest sensitivity to be useful as a potential biomarker for the differential diagnosis.</description><subject>Aberration</subject><subject>Aged</subject><subject>Alveoli</subject><subject>Alveolitis</subject><subject>Bioindicators</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Biomarkers - metabolism</subject><subject>Bronchi - cytology</subject><subject>Bronchi - metabolism</subject><subject>Bronchoalveolar lavage</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchus</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cellular proteins</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Connective tissue diseases</subject><subject>Connective tissues</subject><subject>Development and progression</subject><subject>Diagnosis</subject><subject>Differential diagnosis</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Etiology</subject><subject>Extracellular matrix</subject><subject>Family medical history</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Hypersensitivity</subject><subject>Idiopathic Pulmonary Fibrosis - blood</subject><subject>Idiopathic Pulmonary Fibrosis - diagnosis</subject><subject>Idiopathic Pulmonary Fibrosis - metabolism</subject><subject>Inflammation</subject><subject>Localization</subject><subject>Lung diseases</subject><subject>Lung Diseases, Interstitial - blood</subject><subject>Lung Diseases, Interstitial - diagnosis</subject><subject>Lung Diseases, Interstitial - metabolism</subject><subject>Lungs</subject><subject>Male</subject><subject>Medical diagnosis</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Parenchyma</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>People and Places</subject><subject>Physiological aspects</subject><subject>Pneumonia</subject><subject>Pneumonitis</subject><subject>Population</subject><subject>Proteins</subject><subject>Pulmonary Alveoli - cytology</subject><subject>Pulmonary Alveoli - metabolism</subject><subject>Pulmonary fibrosis</subject><subject>Research and Analysis Methods</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>Rodents</subject><subject>Sensitivity</subject><subject>Serum levels</subject><subject>Sex Factors</subject><subject>Tomography</subject><subject>Uteroglobin - blood</subject><subject>Uteroglobin - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11vFCEUhidGY2v1HxidxMToxa4cGGDmxqTZtLqxSRu_bgkDzC6b2WEERuu_l-1Omx3Ti4YLCDzn5eVwTpa9BDQHwuHDxg2-k-28d52ZI2AlpfhRdgwVwTOGEXl8sD7KnoWwQYiSkrGn2RHmFecl4OPsy7JT3shgdH523XsTgnVd7pp8sQCW2y6_ktGaLob8j43rfKmt62VcW5VfDe3WddL_zc9t7V2w4Xn2pJFtMC_G-ST7cX72ffF5dnH5abk4vZgpjmmc1agiNUGIGWYw1AWrtJaGITCcNLpUuKkZkQVnRa0KVfKy4aBZTRmVkhGKyUn2eq_bty6IMQ9BQEkREAScJ2K5J7STG9F7u00-hZNW3Gw4vxLSR6taI4yuDVQVbbTSRUNwBWXFiOZGUdBY0aT1cbxtqLdGq5QML9uJ6PSks2uxcr8FBVoiypLAu1HAu1-DCVFsbVCmbWVn3HDjuyo4BoCHoICr5HFn681_6P2JGKmVTG-1XeOSRbUTFacFLxAgUpSJmt9DpaHN1qpUX41N-5OA95OAxERzHVdyCEEsv319OHv5c8q-PWDXRrZxHVw7xFSUYQoWe1ClygveNHf_AUjs2uM2G2LXHmJsjxT26vAv74Ju-4H8AzwFCHw</recordid><startdate>20161215</startdate><enddate>20161215</enddate><creator>Buendía-Roldán, Ivette</creator><creator>Ruiz, Víctor</creator><creator>Sierra, Patricia</creator><creator>Montes, Eduardo</creator><creator>Ramírez, Remedios</creator><creator>Vega, Anita</creator><creator>Salgado, Alfonso</creator><creator>Vargas, Mario H</creator><creator>Mejía, Mayra</creator><creator>Pardo, Annie</creator><creator>Selman, Moisés</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>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>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20161215</creationdate><title>Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis</title><author>Buendía-Roldán, Ivette ; Ruiz, Víctor ; Sierra, Patricia ; Montes, Eduardo ; Ramírez, Remedios ; Vega, Anita ; Salgado, Alfonso ; Vargas, Mario H ; Mejía, Mayra ; Pardo, Annie ; Selman, Moisés</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-b093b3006e6e21b469ddae601e73fd8c2fb63a4764bc4c878f71d6b565aa63523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aberration</topic><topic>Aged</topic><topic>Alveoli</topic><topic>Alveolitis</topic><topic>Bioindicators</topic><topic>Biology and Life Sciences</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Biomarkers - metabolism</topic><topic>Bronchi - cytology</topic><topic>Bronchi - metabolism</topic><topic>Bronchoalveolar lavage</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Bronchus</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cellular proteins</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Connective tissue diseases</topic><topic>Connective tissues</topic><topic>Development and progression</topic><topic>Diagnosis</topic><topic>Differential diagnosis</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Etiology</topic><topic>Extracellular matrix</topic><topic>Family medical history</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Hypersensitivity</topic><topic>Idiopathic Pulmonary Fibrosis - blood</topic><topic>Idiopathic Pulmonary Fibrosis - diagnosis</topic><topic>Idiopathic Pulmonary Fibrosis - metabolism</topic><topic>Inflammation</topic><topic>Localization</topic><topic>Lung diseases</topic><topic>Lung Diseases, Interstitial - blood</topic><topic>Lung Diseases, Interstitial - diagnosis</topic><topic>Lung Diseases, Interstitial - metabolism</topic><topic>Lungs</topic><topic>Male</topic><topic>Medical diagnosis</topic><topic>Medicine and Health Sciences</topic><topic>Middle Aged</topic><topic>Parenchyma</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>People and Places</topic><topic>Physiological aspects</topic><topic>Pneumonia</topic><topic>Pneumonitis</topic><topic>Population</topic><topic>Proteins</topic><topic>Pulmonary Alveoli - cytology</topic><topic>Pulmonary Alveoli - metabolism</topic><topic>Pulmonary fibrosis</topic><topic>Research and Analysis Methods</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>Rodents</topic><topic>Sensitivity</topic><topic>Serum levels</topic><topic>Sex Factors</topic><topic>Tomography</topic><topic>Uteroglobin - 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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>Buendía-Roldán, Ivette</au><au>Ruiz, Víctor</au><au>Sierra, Patricia</au><au>Montes, Eduardo</au><au>Ramírez, Remedios</au><au>Vega, Anita</au><au>Salgado, Alfonso</au><au>Vargas, Mario H</au><au>Mejía, Mayra</au><au>Pardo, Annie</au><au>Selman, Moisés</au><au>Morty, Rory Edward</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-12-15</date><risdate>2016</risdate><volume>11</volume><issue>12</issue><spage>e0168552</spage><epage>e0168552</epage><pages>e0168552-e0168552</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology. The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts and finally the excessive accumulation of extracellular matrix with the consequent destruction of the lung parenchyma. CC16 (approved symbol SCGB1A1), a putative anti-inflammatory protein produced by "club" cells in the distal airways, has not been evaluated in IPF lungs. In this study, we determined the serum and bronchoalveolar lavage (BAL) levels as well as the lung cell localization of this protein. Also, we explored the usefulness of serum levels of CC16 for the differential diagnosis of IPF (n = 85), compared with non-IPF interstitial lung diseases [chronic hypersensitivity pneumonitis (cHP; n = 85) and connective tissue diseases (CTD-ILD; n = 85)]. CC16 was significantly increased in serum and BAL fluids of IPF patients and was found not only in club cells but also in alveolar epithelial cells. When compared with non-IPF patients and controls, serum levels were significantly increased (p<0.0001). Sensitivity and specificity for CC16 (cut-off 41ng/mL) were 24% and 90%, positive predictive value 56% and negative predictive value 69%. These findings demonstrate that CC16 is upregulated in IPF patients suggesting that may participate in its pathogenesis. Although higher than the serum levels of non-IPF patients it shows modest sensitivity to be useful as a potential biomarker for the differential diagnosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27977812</pmid><doi>10.1371/journal.pone.0168552</doi><tpages>e0168552</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-12, Vol.11 (12), p.e0168552-e0168552 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1850130177 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Aberration Aged Alveoli Alveolitis Bioindicators Biology and Life Sciences Biomarkers Biomarkers - blood Biomarkers - metabolism Bronchi - cytology Bronchi - metabolism Bronchoalveolar lavage Bronchoalveolar Lavage Fluid - chemistry Bronchus Cell migration Cell proliferation Cellular proteins Chronic obstructive pulmonary disease Connective tissue diseases Connective tissues Development and progression Diagnosis Differential diagnosis Epithelial cells Epithelial Cells - metabolism Etiology Extracellular matrix Family medical history Female Fibroblasts Fibrosis Gene expression Genetic aspects Humans Hypersensitivity Idiopathic Pulmonary Fibrosis - blood Idiopathic Pulmonary Fibrosis - diagnosis Idiopathic Pulmonary Fibrosis - metabolism Inflammation Localization Lung diseases Lung Diseases, Interstitial - blood Lung Diseases, Interstitial - diagnosis Lung Diseases, Interstitial - metabolism Lungs Male Medical diagnosis Medicine and Health Sciences Middle Aged Parenchyma Pathogenesis Patients People and Places Physiological aspects Pneumonia Pneumonitis Population Proteins Pulmonary Alveoli - cytology Pulmonary Alveoli - metabolism Pulmonary fibrosis Research and Analysis Methods Rheumatoid arthritis Rheumatology Rodents Sensitivity Serum levels Sex Factors Tomography Uteroglobin - blood Uteroglobin - metabolism |
| title | Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis |
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