A study of genes encoding cytokines (IL6, IL10, TNF), cytokine receptors (IL6R, IL6ST), and glucocorticoid receptor (NR3C1) and susceptibility to bronchopulmonary dysplasia
Bronchopulmonary dysplasia (BPD) is a common chronic lung disease associated with very preterm birth. The major risk factors include lung inflammation and lung immaturity. In addition, genetic factors play an important role in susceptibility to moderate-to-severe BPD. In this study, the aim was to i...
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| Veröffentlicht in: | BMC genetics 2014-11, Vol.15 (1), p.120-120, Article 120 |
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| creator | Huusko, Johanna M Karjalainen, Minna K Mahlman, Mari Haataja, Ritva Kari, M Anneli Andersson, Sture Toldi, Gergely Tammela, Outi Rämet, Mika Lavoie, Pascal M Hallman, Mikko |
| description | Bronchopulmonary dysplasia (BPD) is a common chronic lung disease associated with very preterm birth. The major risk factors include lung inflammation and lung immaturity. In addition, genetic factors play an important role in susceptibility to moderate-to-severe BPD. In this study, the aim was to investigate whether common polymorphisms of specific genes that are involved in inflammation or differentiation of the lung have influence on BPD susceptibility.
Genes encoding interleukin-6 (IL6) and its receptors (IL6R and IL6ST), IL-10 (IL10), tumor necrosis factor (TNF), and glucocorticoid receptor (NR3C1) were assessed for associations with moderate-to-severe BPD susceptibility. Five IL6, nine IL6R, four IL6ST, one IL10, two TNF, and 23 NR3C1 single nucleotide polymorphisms (SNPs) were analyzed in very preterm infants born in northern Finland (56 cases and 197 controls) and Canada (58 cases and 68 controls). IL-6, TNF and gp130 contents in umbilical cord blood, collected from very preterm infants, were studied for associations with the polymorphisms. Epistasis (i.e., interactions between SNPs in BPD susceptibility) was also examined. SNPs showing suggestive associations were analyzed in additional replication populations from Finland (39 cases and 188 controls) and Hungary (29 cases and 40 controls).
None of the studied SNPs were associated with BPD nor were the IL6, TNF or IL6ST SNPs associated with cord blood IL-6, TNF and gp130, respectively. However, epistasis analysis suggested that SNPs in IL6ST and IL10 were associated interactively with risk of BPD in the northern Finnish population; however, this finding did not remain significant after correction for multiple testing and the finding was not replicated in the other populations.
We conclude that the analyzed SNPs within IL6, IL6R, IL6ST, IL10, TNF, and NR3C1 were not associated with BPD. Furthermore, there was no evidence that the studied SNPs directly contribute to the cord blood protein contents. |
| doi_str_mv | 10.1186/s12881-014-0120-7 |
| format | Article |
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Genes encoding interleukin-6 (IL6) and its receptors (IL6R and IL6ST), IL-10 (IL10), tumor necrosis factor (TNF), and glucocorticoid receptor (NR3C1) were assessed for associations with moderate-to-severe BPD susceptibility. Five IL6, nine IL6R, four IL6ST, one IL10, two TNF, and 23 NR3C1 single nucleotide polymorphisms (SNPs) were analyzed in very preterm infants born in northern Finland (56 cases and 197 controls) and Canada (58 cases and 68 controls). IL-6, TNF and gp130 contents in umbilical cord blood, collected from very preterm infants, were studied for associations with the polymorphisms. Epistasis (i.e., interactions between SNPs in BPD susceptibility) was also examined. SNPs showing suggestive associations were analyzed in additional replication populations from Finland (39 cases and 188 controls) and Hungary (29 cases and 40 controls).
None of the studied SNPs were associated with BPD nor were the IL6, TNF or IL6ST SNPs associated with cord blood IL-6, TNF and gp130, respectively. However, epistasis analysis suggested that SNPs in IL6ST and IL10 were associated interactively with risk of BPD in the northern Finnish population; however, this finding did not remain significant after correction for multiple testing and the finding was not replicated in the other populations.
We conclude that the analyzed SNPs within IL6, IL6R, IL6ST, IL10, TNF, and NR3C1 were not associated with BPD. Furthermore, there was no evidence that the studied SNPs directly contribute to the cord blood protein contents.</description><identifier>ISSN: 1471-2350</identifier><identifier>ISSN: 1471-2156</identifier><identifier>EISSN: 1471-2350</identifier><identifier>EISSN: 1471-2156</identifier><identifier>DOI: 10.1186/s12881-014-0120-7</identifier><identifier>PMID: 25409741</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Bronchopulmonary Dysplasia - genetics ; Bronchopulmonary Dysplasia - pathology ; Case-Control Studies ; Cytokine Receptor gp130 - genetics ; Cytokines - genetics ; Disease Susceptibility ; Epistasis, Genetic ; Genes ; Genotype ; Gestational Age ; Hospitals ; Humans ; Infant, Newborn ; Interleukin-10 - genetics ; Interleukin-6 - genetics ; Linkage Disequilibrium ; Medical research ; Polymorphism, Single Nucleotide ; Receptors, Cytokine - genetics ; Receptors, Glucocorticoid - genetics ; Receptors, Interleukin-6 - genetics ; Studies ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>BMC genetics, 2014-11, Vol.15 (1), p.120-120, Article 120</ispartof><rights>2014 Huusko et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Huusko et al.; licensee BioMed Central Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-e5d02e50bf7cf7119f172a4e126f52ec2bfda7b41bf635cfe4254f7e2f0bebd63</citedby><cites>FETCH-LOGICAL-c460t-e5d02e50bf7cf7119f172a4e126f52ec2bfda7b41bf635cfe4254f7e2f0bebd63</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/PMC4258941/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258941/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25409741$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huusko, Johanna M</creatorcontrib><creatorcontrib>Karjalainen, Minna K</creatorcontrib><creatorcontrib>Mahlman, Mari</creatorcontrib><creatorcontrib>Haataja, Ritva</creatorcontrib><creatorcontrib>Kari, M Anneli</creatorcontrib><creatorcontrib>Andersson, Sture</creatorcontrib><creatorcontrib>Toldi, Gergely</creatorcontrib><creatorcontrib>Tammela, Outi</creatorcontrib><creatorcontrib>Rämet, Mika</creatorcontrib><creatorcontrib>Lavoie, Pascal M</creatorcontrib><creatorcontrib>Hallman, Mikko</creatorcontrib><creatorcontrib>Gen-BPD Study Group</creatorcontrib><title>A study of genes encoding cytokines (IL6, IL10, TNF), cytokine receptors (IL6R, IL6ST), and glucocorticoid receptor (NR3C1) and susceptibility to bronchopulmonary dysplasia</title><title>BMC genetics</title><addtitle>BMC Med Genet</addtitle><description>Bronchopulmonary dysplasia (BPD) is a common chronic lung disease associated with very preterm birth. The major risk factors include lung inflammation and lung immaturity. In addition, genetic factors play an important role in susceptibility to moderate-to-severe BPD. In this study, the aim was to investigate whether common polymorphisms of specific genes that are involved in inflammation or differentiation of the lung have influence on BPD susceptibility.
Genes encoding interleukin-6 (IL6) and its receptors (IL6R and IL6ST), IL-10 (IL10), tumor necrosis factor (TNF), and glucocorticoid receptor (NR3C1) were assessed for associations with moderate-to-severe BPD susceptibility. Five IL6, nine IL6R, four IL6ST, one IL10, two TNF, and 23 NR3C1 single nucleotide polymorphisms (SNPs) were analyzed in very preterm infants born in northern Finland (56 cases and 197 controls) and Canada (58 cases and 68 controls). IL-6, TNF and gp130 contents in umbilical cord blood, collected from very preterm infants, were studied for associations with the polymorphisms. Epistasis (i.e., interactions between SNPs in BPD susceptibility) was also examined. SNPs showing suggestive associations were analyzed in additional replication populations from Finland (39 cases and 188 controls) and Hungary (29 cases and 40 controls).
None of the studied SNPs were associated with BPD nor were the IL6, TNF or IL6ST SNPs associated with cord blood IL-6, TNF and gp130, respectively. However, epistasis analysis suggested that SNPs in IL6ST and IL10 were associated interactively with risk of BPD in the northern Finnish population; however, this finding did not remain significant after correction for multiple testing and the finding was not replicated in the other populations.
We conclude that the analyzed SNPs within IL6, IL6R, IL6ST, IL10, TNF, and NR3C1 were not associated with BPD. Furthermore, there was no evidence that the studied SNPs directly contribute to the cord blood protein contents.</description><subject>Bronchopulmonary Dysplasia - genetics</subject><subject>Bronchopulmonary Dysplasia - pathology</subject><subject>Case-Control Studies</subject><subject>Cytokine Receptor gp130 - genetics</subject><subject>Cytokines - genetics</subject><subject>Disease Susceptibility</subject><subject>Epistasis, Genetic</subject><subject>Genes</subject><subject>Genotype</subject><subject>Gestational Age</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-6 - genetics</subject><subject>Linkage Disequilibrium</subject><subject>Medical research</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, Cytokine - genetics</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Receptors, Interleukin-6 - genetics</subject><subject>Studies</subject><subject>Tumor Necrosis Factor-alpha - 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genetics</topic><topic>Bronchopulmonary Dysplasia - pathology</topic><topic>Case-Control Studies</topic><topic>Cytokine Receptor gp130 - genetics</topic><topic>Cytokines - genetics</topic><topic>Disease Susceptibility</topic><topic>Epistasis, Genetic</topic><topic>Genes</topic><topic>Genotype</topic><topic>Gestational Age</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-6 - genetics</topic><topic>Linkage Disequilibrium</topic><topic>Medical research</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Receptors, Cytokine - genetics</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Receptors, Interleukin-6 - genetics</topic><topic>Studies</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huusko, Johanna M</creatorcontrib><creatorcontrib>Karjalainen, Minna K</creatorcontrib><creatorcontrib>Mahlman, Mari</creatorcontrib><creatorcontrib>Haataja, Ritva</creatorcontrib><creatorcontrib>Kari, M Anneli</creatorcontrib><creatorcontrib>Andersson, Sture</creatorcontrib><creatorcontrib>Toldi, Gergely</creatorcontrib><creatorcontrib>Tammela, Outi</creatorcontrib><creatorcontrib>Rämet, Mika</creatorcontrib><creatorcontrib>Lavoie, Pascal M</creatorcontrib><creatorcontrib>Hallman, Mikko</creatorcontrib><creatorcontrib>Gen-BPD Study Group</creatorcontrib><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>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huusko, Johanna M</au><au>Karjalainen, Minna K</au><au>Mahlman, Mari</au><au>Haataja, Ritva</au><au>Kari, M Anneli</au><au>Andersson, Sture</au><au>Toldi, Gergely</au><au>Tammela, Outi</au><au>Rämet, Mika</au><au>Lavoie, Pascal M</au><au>Hallman, Mikko</au><aucorp>Gen-BPD Study Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A study of genes encoding cytokines (IL6, IL10, TNF), cytokine receptors (IL6R, IL6ST), and glucocorticoid receptor (NR3C1) and susceptibility to bronchopulmonary dysplasia</atitle><jtitle>BMC genetics</jtitle><addtitle>BMC Med Genet</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>15</volume><issue>1</issue><spage>120</spage><epage>120</epage><pages>120-120</pages><artnum>120</artnum><issn>1471-2350</issn><issn>1471-2156</issn><eissn>1471-2350</eissn><eissn>1471-2156</eissn><abstract>Bronchopulmonary dysplasia (BPD) is a common chronic lung disease associated with very preterm birth. The major risk factors include lung inflammation and lung immaturity. In addition, genetic factors play an important role in susceptibility to moderate-to-severe BPD. In this study, the aim was to investigate whether common polymorphisms of specific genes that are involved in inflammation or differentiation of the lung have influence on BPD susceptibility.
Genes encoding interleukin-6 (IL6) and its receptors (IL6R and IL6ST), IL-10 (IL10), tumor necrosis factor (TNF), and glucocorticoid receptor (NR3C1) were assessed for associations with moderate-to-severe BPD susceptibility. Five IL6, nine IL6R, four IL6ST, one IL10, two TNF, and 23 NR3C1 single nucleotide polymorphisms (SNPs) were analyzed in very preterm infants born in northern Finland (56 cases and 197 controls) and Canada (58 cases and 68 controls). IL-6, TNF and gp130 contents in umbilical cord blood, collected from very preterm infants, were studied for associations with the polymorphisms. Epistasis (i.e., interactions between SNPs in BPD susceptibility) was also examined. SNPs showing suggestive associations were analyzed in additional replication populations from Finland (39 cases and 188 controls) and Hungary (29 cases and 40 controls).
None of the studied SNPs were associated with BPD nor were the IL6, TNF or IL6ST SNPs associated with cord blood IL-6, TNF and gp130, respectively. However, epistasis analysis suggested that SNPs in IL6ST and IL10 were associated interactively with risk of BPD in the northern Finnish population; however, this finding did not remain significant after correction for multiple testing and the finding was not replicated in the other populations.
We conclude that the analyzed SNPs within IL6, IL6R, IL6ST, IL10, TNF, and NR3C1 were not associated with BPD. Furthermore, there was no evidence that the studied SNPs directly contribute to the cord blood protein contents.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>25409741</pmid><doi>10.1186/s12881-014-0120-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Bronchopulmonary Dysplasia - genetics Bronchopulmonary Dysplasia - pathology Case-Control Studies Cytokine Receptor gp130 - genetics Cytokines - genetics Disease Susceptibility Epistasis, Genetic Genes Genotype Gestational Age Hospitals Humans Infant, Newborn Interleukin-10 - genetics Interleukin-6 - genetics Linkage Disequilibrium Medical research Polymorphism, Single Nucleotide Receptors, Cytokine - genetics Receptors, Glucocorticoid - genetics Receptors, Interleukin-6 - genetics Studies Tumor Necrosis Factor-alpha - genetics |
| title | A study of genes encoding cytokines (IL6, IL10, TNF), cytokine receptors (IL6R, IL6ST), and glucocorticoid receptor (NR3C1) and susceptibility to bronchopulmonary dysplasia |
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