Protective effects of elafin against adult asthma
Background: Elafin inhibits serine proteases, such as human neutrophil elastase and proteinase 3, to prevent excessive damage during inflammation. However, the relationship between elafin and asthma is still unclear. Microarray technology was used to evaluate smoking- and asthma-related biomarkers i...
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| creator | Tsai, Yi-Shan Tseng, Yu-Ting Chen, Pei-Shih Lin, Meng-Chih Wu, Chao-Chien Huang, Ming-Shyan Wang, Chin-Chou Chen, Kang-Shin Lin, Yuan-Chung Wang, Tsu-Nai |
| description | Background: Elafin inhibits serine proteases, such as human neutrophil elastase and proteinase 3, to prevent excessive damage during inflammation. However, the relationship between elafin and asthma is still unclear. Microarray technology was used to evaluate smoking- and
asthma-related biomarkers in a discovery-driven manner. We identified candidate genes, e.g., proteinase inhibitor 3 (PI3), related to asthma and smoking from gene expression microarray data sets and evaluated their potential as biomarkers for asthma. Methods: We used human
genome microarray data sets from smoking- and asthma-related gene expression data sets and performed real-time quantitative polymerase chain reaction to measure and validate differences in gene expression. We also recruited adult patients with asthma and age- and sex-matched control patients
who were administered a structured questionnaire and evaluated for lung function and plasma elafin levels, which are encoded by the PI3 gene. Results: Six significantly altered candidate genes, PI3, protein kinase C iota, phosphoserine phosphatase, IQ motif-containing GTPase
activating protein 1, interleukin 13 receptor α 1, and signal transducing adaptor molecule SH3 domain and ITAM motif 2, were identified from comparisons across the four asthma- and four smoking-related data sets included in this study. An in vitro study of human airway epithelial cells
(A549) and a human monocytic cell line (THP-1) demonstrated that PI3 messenger RNA levels were significantly altered by nicotine exposure. Elafin concentration was significantly higher in control patients than in patients with asthma (p < 0.001). The plasma elafin concentration in the highest
quartile (≥12.69 ng/mL) was inversely associated with asthma (adjusted odds ratio 0.122 [95% confidence interval, 0.053-0.278]) compared with the lowest quartile ( |
| doi_str_mv | 10.2500/aap.2016.37.3932 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1770224139</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><ingid>ocean/aap/2016/00000037/00000002/art00001</ingid><sourcerecordid>1787984618</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-ea913ccd26900bd06c1dbb4a34a7c38e66b5c434e723897978fb2e2980c50c0a3</originalsourceid><addsrcrecordid>eNqNkD1PwzAQhi0EoqWwM6GMLAnnj9jOWFV8SZVggNm6OE5JlSYlTpD49zikwMoNvnd47rX0EHJJIWEpwA3iPmFAZcJVwjPOjsicpjyLJQdxHDJoHaeCshk5834LQAWX8pTMmAwwlemc0Oeu7Z3tqw8XubIMyUdtGbkay6qJcINV4_sIi6EOr-_fdnhOTkqsvbs47AV5vbt9WT3E66f7x9VyHVueQR87zCi3tghfAeQFSEuLPBfIBSrLtZMyT63gwinGdaYypcucOZZpsClYQL4g11PvvmvfB-d7s6u8dXWNjWsHb6jSKtNCUv0PVAFjggZFCwITarvW-86VZt9VO-w-DQUzOjXBqRmdGq7M6DScXB3ah3znit-DH4kBWE5A1Wxc06PZtkPXBDemtQ6bv0b4ntA7BWAGu34MlH8B-m-E8w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1770224139</pqid></control><display><type>article</type><title>Protective effects of elafin against adult asthma</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Tsai, Yi-Shan ; Tseng, Yu-Ting ; Chen, Pei-Shih ; Lin, Meng-Chih ; Wu, Chao-Chien ; Huang, Ming-Shyan ; Wang, Chin-Chou ; Chen, Kang-Shin ; Lin, Yuan-Chung ; Wang, Tsu-Nai</creator><creatorcontrib>Tsai, Yi-Shan ; Tseng, Yu-Ting ; Chen, Pei-Shih ; Lin, Meng-Chih ; Wu, Chao-Chien ; Huang, Ming-Shyan ; Wang, Chin-Chou ; Chen, Kang-Shin ; Lin, Yuan-Chung ; Wang, Tsu-Nai</creatorcontrib><description>Background: Elafin inhibits serine proteases, such as human neutrophil elastase and proteinase 3, to prevent excessive damage during inflammation. However, the relationship between elafin and asthma is still unclear. Microarray technology was used to evaluate smoking- and
asthma-related biomarkers in a discovery-driven manner. We identified candidate genes, e.g., proteinase inhibitor 3 (PI3), related to asthma and smoking from gene expression microarray data sets and evaluated their potential as biomarkers for asthma. Methods: We used human
genome microarray data sets from smoking- and asthma-related gene expression data sets and performed real-time quantitative polymerase chain reaction to measure and validate differences in gene expression. We also recruited adult patients with asthma and age- and sex-matched control patients
who were administered a structured questionnaire and evaluated for lung function and plasma elafin levels, which are encoded by the PI3 gene. Results: Six significantly altered candidate genes, PI3, protein kinase C iota, phosphoserine phosphatase, IQ motif-containing GTPase
activating protein 1, interleukin 13 receptor α 1, and signal transducing adaptor molecule SH3 domain and ITAM motif 2, were identified from comparisons across the four asthma- and four smoking-related data sets included in this study. An in vitro study of human airway epithelial cells
(A549) and a human monocytic cell line (THP-1) demonstrated that PI3 messenger RNA levels were significantly altered by nicotine exposure. Elafin concentration was significantly higher in control patients than in patients with asthma (p < 0.001). The plasma elafin concentration in the highest
quartile (≥12.69 ng/mL) was inversely associated with asthma (adjusted odds ratio 0.122 [95% confidence interval, 0.053-0.278]) compared with the lowest quartile (<5.82 ng/mL) after adjusting for age, sex, smoking status, waist-to-hip ratio, percentage predicted forced expiratory
volume in 1 second, cockroaches in the home, incense burning, and family history. Conclusion: Our study revealed that high elafin levels identified in smoking- and asthma-related microarray data sets and an epidemiologic study significantly reduced the risk of asthma. Further
studies of elafin as a potential therapy for asthma are warranted.</description><identifier>ISSN: 1088-5412</identifier><identifier>EISSN: 1539-6304</identifier><identifier>DOI: 10.2500/aap.2016.37.3932</identifier><identifier>PMID: 26932165</identifier><language>eng</language><publisher>United States: OceanSide Publications, Inc</publisher><subject>Adult ; Asthma ; Asthma - diagnosis ; Asthma - genetics ; Asthma - immunology ; Asthma - metabolism ; Biomarkers ; Cell Line ; Computational Biology - methods ; Elafin - blood ; Elafin - genetics ; Elafin - metabolism ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Immunoglobulin E - blood ; Immunoglobulin E - immunology ; Male ; Middle Aged ; Odds Ratio ; Pi3 Gene ; Plasma Elafin ; Protease Inhibitors - blood ; Protease Inhibitors - metabolism ; Respiratory Function Tests ; Risk Factors ; Smoking</subject><ispartof>Allergy and asthma proceedings, 2016-03, Vol.37 (2), p.e15-e24</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-ea913ccd26900bd06c1dbb4a34a7c38e66b5c434e723897978fb2e2980c50c0a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26932165$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsai, Yi-Shan</creatorcontrib><creatorcontrib>Tseng, Yu-Ting</creatorcontrib><creatorcontrib>Chen, Pei-Shih</creatorcontrib><creatorcontrib>Lin, Meng-Chih</creatorcontrib><creatorcontrib>Wu, Chao-Chien</creatorcontrib><creatorcontrib>Huang, Ming-Shyan</creatorcontrib><creatorcontrib>Wang, Chin-Chou</creatorcontrib><creatorcontrib>Chen, Kang-Shin</creatorcontrib><creatorcontrib>Lin, Yuan-Chung</creatorcontrib><creatorcontrib>Wang, Tsu-Nai</creatorcontrib><title>Protective effects of elafin against adult asthma</title><title>Allergy and asthma proceedings</title><addtitle>Allergy Asthma Proc</addtitle><description>Background: Elafin inhibits serine proteases, such as human neutrophil elastase and proteinase 3, to prevent excessive damage during inflammation. However, the relationship between elafin and asthma is still unclear. Microarray technology was used to evaluate smoking- and
asthma-related biomarkers in a discovery-driven manner. We identified candidate genes, e.g., proteinase inhibitor 3 (PI3), related to asthma and smoking from gene expression microarray data sets and evaluated their potential as biomarkers for asthma. Methods: We used human
genome microarray data sets from smoking- and asthma-related gene expression data sets and performed real-time quantitative polymerase chain reaction to measure and validate differences in gene expression. We also recruited adult patients with asthma and age- and sex-matched control patients
who were administered a structured questionnaire and evaluated for lung function and plasma elafin levels, which are encoded by the PI3 gene. Results: Six significantly altered candidate genes, PI3, protein kinase C iota, phosphoserine phosphatase, IQ motif-containing GTPase
activating protein 1, interleukin 13 receptor α 1, and signal transducing adaptor molecule SH3 domain and ITAM motif 2, were identified from comparisons across the four asthma- and four smoking-related data sets included in this study. An in vitro study of human airway epithelial cells
(A549) and a human monocytic cell line (THP-1) demonstrated that PI3 messenger RNA levels were significantly altered by nicotine exposure. Elafin concentration was significantly higher in control patients than in patients with asthma (p < 0.001). The plasma elafin concentration in the highest
quartile (≥12.69 ng/mL) was inversely associated with asthma (adjusted odds ratio 0.122 [95% confidence interval, 0.053-0.278]) compared with the lowest quartile (<5.82 ng/mL) after adjusting for age, sex, smoking status, waist-to-hip ratio, percentage predicted forced expiratory
volume in 1 second, cockroaches in the home, incense burning, and family history. Conclusion: Our study revealed that high elafin levels identified in smoking- and asthma-related microarray data sets and an epidemiologic study significantly reduced the risk of asthma. Further
studies of elafin as a potential therapy for asthma are warranted.</description><subject>Adult</subject><subject>Asthma</subject><subject>Asthma - diagnosis</subject><subject>Asthma - genetics</subject><subject>Asthma - immunology</subject><subject>Asthma - metabolism</subject><subject>Biomarkers</subject><subject>Cell Line</subject><subject>Computational Biology - methods</subject><subject>Elafin - blood</subject><subject>Elafin - genetics</subject><subject>Elafin - metabolism</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Immunoglobulin E - blood</subject><subject>Immunoglobulin E - immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Pi3 Gene</subject><subject>Plasma Elafin</subject><subject>Protease Inhibitors - blood</subject><subject>Protease Inhibitors - metabolism</subject><subject>Respiratory Function Tests</subject><subject>Risk Factors</subject><subject>Smoking</subject><issn>1088-5412</issn><issn>1539-6304</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkD1PwzAQhi0EoqWwM6GMLAnnj9jOWFV8SZVggNm6OE5JlSYlTpD49zikwMoNvnd47rX0EHJJIWEpwA3iPmFAZcJVwjPOjsicpjyLJQdxHDJoHaeCshk5834LQAWX8pTMmAwwlemc0Oeu7Z3tqw8XubIMyUdtGbkay6qJcINV4_sIi6EOr-_fdnhOTkqsvbs47AV5vbt9WT3E66f7x9VyHVueQR87zCi3tghfAeQFSEuLPBfIBSrLtZMyT63gwinGdaYypcucOZZpsClYQL4g11PvvmvfB-d7s6u8dXWNjWsHb6jSKtNCUv0PVAFjggZFCwITarvW-86VZt9VO-w-DQUzOjXBqRmdGq7M6DScXB3ah3znit-DH4kBWE5A1Wxc06PZtkPXBDemtQ6bv0b4ntA7BWAGu34MlH8B-m-E8w</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Tsai, Yi-Shan</creator><creator>Tseng, Yu-Ting</creator><creator>Chen, Pei-Shih</creator><creator>Lin, Meng-Chih</creator><creator>Wu, Chao-Chien</creator><creator>Huang, Ming-Shyan</creator><creator>Wang, Chin-Chou</creator><creator>Chen, Kang-Shin</creator><creator>Lin, Yuan-Chung</creator><creator>Wang, Tsu-Nai</creator><general>OceanSide Publications, Inc</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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20160301</creationdate><title>Protective effects of elafin against adult asthma</title><author>Tsai, Yi-Shan ; Tseng, Yu-Ting ; Chen, Pei-Shih ; Lin, Meng-Chih ; Wu, Chao-Chien ; Huang, Ming-Shyan ; Wang, Chin-Chou ; Chen, Kang-Shin ; Lin, Yuan-Chung ; Wang, Tsu-Nai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-ea913ccd26900bd06c1dbb4a34a7c38e66b5c434e723897978fb2e2980c50c0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Asthma</topic><topic>Asthma - diagnosis</topic><topic>Asthma - genetics</topic><topic>Asthma - immunology</topic><topic>Asthma - metabolism</topic><topic>Biomarkers</topic><topic>Cell Line</topic><topic>Computational Biology - methods</topic><topic>Elafin - blood</topic><topic>Elafin - genetics</topic><topic>Elafin - metabolism</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Immunoglobulin E - blood</topic><topic>Immunoglobulin E - immunology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Pi3 Gene</topic><topic>Plasma Elafin</topic><topic>Protease Inhibitors - blood</topic><topic>Protease Inhibitors - metabolism</topic><topic>Respiratory Function Tests</topic><topic>Risk Factors</topic><topic>Smoking</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsai, Yi-Shan</creatorcontrib><creatorcontrib>Tseng, Yu-Ting</creatorcontrib><creatorcontrib>Chen, Pei-Shih</creatorcontrib><creatorcontrib>Lin, Meng-Chih</creatorcontrib><creatorcontrib>Wu, Chao-Chien</creatorcontrib><creatorcontrib>Huang, Ming-Shyan</creatorcontrib><creatorcontrib>Wang, Chin-Chou</creatorcontrib><creatorcontrib>Chen, Kang-Shin</creatorcontrib><creatorcontrib>Lin, Yuan-Chung</creatorcontrib><creatorcontrib>Wang, Tsu-Nai</creatorcontrib><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>Allergy and asthma proceedings</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsai, Yi-Shan</au><au>Tseng, Yu-Ting</au><au>Chen, Pei-Shih</au><au>Lin, Meng-Chih</au><au>Wu, Chao-Chien</au><au>Huang, Ming-Shyan</au><au>Wang, Chin-Chou</au><au>Chen, Kang-Shin</au><au>Lin, Yuan-Chung</au><au>Wang, Tsu-Nai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effects of elafin against adult asthma</atitle><jtitle>Allergy and asthma proceedings</jtitle><addtitle>Allergy Asthma Proc</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>37</volume><issue>2</issue><spage>e15</spage><epage>e24</epage><pages>e15-e24</pages><issn>1088-5412</issn><eissn>1539-6304</eissn><abstract>Background: Elafin inhibits serine proteases, such as human neutrophil elastase and proteinase 3, to prevent excessive damage during inflammation. However, the relationship between elafin and asthma is still unclear. Microarray technology was used to evaluate smoking- and
asthma-related biomarkers in a discovery-driven manner. We identified candidate genes, e.g., proteinase inhibitor 3 (PI3), related to asthma and smoking from gene expression microarray data sets and evaluated their potential as biomarkers for asthma. Methods: We used human
genome microarray data sets from smoking- and asthma-related gene expression data sets and performed real-time quantitative polymerase chain reaction to measure and validate differences in gene expression. We also recruited adult patients with asthma and age- and sex-matched control patients
who were administered a structured questionnaire and evaluated for lung function and plasma elafin levels, which are encoded by the PI3 gene. Results: Six significantly altered candidate genes, PI3, protein kinase C iota, phosphoserine phosphatase, IQ motif-containing GTPase
activating protein 1, interleukin 13 receptor α 1, and signal transducing adaptor molecule SH3 domain and ITAM motif 2, were identified from comparisons across the four asthma- and four smoking-related data sets included in this study. An in vitro study of human airway epithelial cells
(A549) and a human monocytic cell line (THP-1) demonstrated that PI3 messenger RNA levels were significantly altered by nicotine exposure. Elafin concentration was significantly higher in control patients than in patients with asthma (p < 0.001). The plasma elafin concentration in the highest
quartile (≥12.69 ng/mL) was inversely associated with asthma (adjusted odds ratio 0.122 [95% confidence interval, 0.053-0.278]) compared with the lowest quartile (<5.82 ng/mL) after adjusting for age, sex, smoking status, waist-to-hip ratio, percentage predicted forced expiratory
volume in 1 second, cockroaches in the home, incense burning, and family history. Conclusion: Our study revealed that high elafin levels identified in smoking- and asthma-related microarray data sets and an epidemiologic study significantly reduced the risk of asthma. Further
studies of elafin as a potential therapy for asthma are warranted.</abstract><cop>United States</cop><pub>OceanSide Publications, Inc</pub><pmid>26932165</pmid><doi>10.2500/aap.2016.37.3932</doi><tpages>10</tpages></addata></record> |
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| subjects | Adult Asthma Asthma - diagnosis Asthma - genetics Asthma - immunology Asthma - metabolism Biomarkers Cell Line Computational Biology - methods Elafin - blood Elafin - genetics Elafin - metabolism Female Gene Expression Profiling Gene Expression Regulation Humans Immunoglobulin E - blood Immunoglobulin E - immunology Male Middle Aged Odds Ratio Pi3 Gene Plasma Elafin Protease Inhibitors - blood Protease Inhibitors - metabolism Respiratory Function Tests Risk Factors Smoking |
| title | Protective effects of elafin against adult asthma |
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