A polymorphism in the IL11 gene is associated with ulcerative colitis
Inflammatory bowel diseases (IBD) are multifactorial disorders characterised by the host's inability to limit the inflammatory response to luminal antigens. The association of polymorphisms in the CARD15 gene with Crohn's disease (CD) demonstrates the relevance of activated transcription f...
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Veröffentlicht in: | Genes and immunity 2002-12, Vol.3 (8), p.494-496 |
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description | Inflammatory bowel diseases (IBD) are multifactorial disorders characterised by the host's inability to limit the inflammatory response to luminal antigens. The association of polymorphisms in the CARD15 gene with Crohn's disease (CD) demonstrates the relevance of activated transcription factor NF
κ
B in mononuclear cells. Interleukin 11 (IL11) mediates anti-inflammatory effects and is able to downregulate LPS-induced NF
κ
B activation. The
IL11
gene is therefore a good candidate involved in genetic predisposition to IBD. To evaluate the role of the
IL11
gene in IBD, two polymorphisms, including a dinucleotide repeat in the promoter region, have been genotyped in 222 patients with CD, 152 patients with ulcerative colitis (UC) and 400 healthy controls. PCR-SSCP analysis of the coding region revealed a single polymorphism in exon 4 leading to an amino acid exchange (G335A; R112H), not significantly associated with either disease. Dinucleotide repeat frequencies of the
IL11.A1
allele and of
IL11.A1
homozygous individuals were significantly increased among the patients with UC (
P |
doi_str_mv | 10.1038/sj.gene.6363897 |
format | Article |
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κ
B in mononuclear cells. Interleukin 11 (IL11) mediates anti-inflammatory effects and is able to downregulate LPS-induced NF
κ
B activation. The
IL11
gene is therefore a good candidate involved in genetic predisposition to IBD. To evaluate the role of the
IL11
gene in IBD, two polymorphisms, including a dinucleotide repeat in the promoter region, have been genotyped in 222 patients with CD, 152 patients with ulcerative colitis (UC) and 400 healthy controls. PCR-SSCP analysis of the coding region revealed a single polymorphism in exon 4 leading to an amino acid exchange (G335A; R112H), not significantly associated with either disease. Dinucleotide repeat frequencies of the
IL11.A1
allele and of
IL11.A1
homozygous individuals were significantly increased among the patients with UC (
P
<0.002 and (
P
<0.003, respectively) but not with CD. Altered expression of
IL11
appears to be involved in the genetic predisposition of UC.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6363897</identifier><identifier>PMID: 12486609</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Alleles ; Amino acids ; Antigens ; Biomedical and Life Sciences ; Biomedicine ; brief-communication ; Cancer Research ; Colitis, Ulcerative - genetics ; Crohn's disease ; Dinucleotide Repeats - genetics ; DNA binding proteins ; Gene Expression ; Gene polymorphism ; Genetic aspects ; Genetic polymorphisms ; Genotype ; Health aspects ; Human Genetics ; Humans ; Immunology ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Interleukin 1 ; Interleukin 11 ; Interleukin-11 - genetics ; Leukocytes (mononuclear) ; Lipopolysaccharides ; NF-κB protein ; Physiological aspects ; Polymorphism ; Polymorphism, Genetic ; Polymorphism, Single-Stranded Conformational ; Promoter Regions, Genetic - immunology ; Risk factors ; Ulcerative colitis</subject><ispartof>Genes and immunity, 2002-12, Vol.3 (8), p.494-496</ispartof><rights>Macmillan Publishers Limited 2002</rights><rights>COPYRIGHT 2002 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2002</rights><rights>Macmillan Publishers Limited 2002.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c564t-99f72c49256f9450c67e406e2b3b9841c1be0a136ad7f76ed4fa5d89f7151e793</citedby><cites>FETCH-LOGICAL-c564t-99f72c49256f9450c67e406e2b3b9841c1be0a136ad7f76ed4fa5d89f7151e793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.gene.6363897$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6363897$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12486609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klein, W</creatorcontrib><creatorcontrib>Tromm, A</creatorcontrib><creatorcontrib>Griga, T</creatorcontrib><creatorcontrib>Fricke, H</creatorcontrib><creatorcontrib>Folwaczny, C</creatorcontrib><creatorcontrib>Hocke, M</creatorcontrib><creatorcontrib>Eitner, K</creatorcontrib><creatorcontrib>Marx, M</creatorcontrib><creatorcontrib>Duerig, N</creatorcontrib><creatorcontrib>Epplen, J T</creatorcontrib><title>A polymorphism in the IL11 gene is associated with ulcerative colitis</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Inflammatory bowel diseases (IBD) are multifactorial disorders characterised by the host's inability to limit the inflammatory response to luminal antigens. The association of polymorphisms in the CARD15 gene with Crohn's disease (CD) demonstrates the relevance of activated transcription factor NF
κ
B in mononuclear cells. Interleukin 11 (IL11) mediates anti-inflammatory effects and is able to downregulate LPS-induced NF
κ
B activation. The
IL11
gene is therefore a good candidate involved in genetic predisposition to IBD. To evaluate the role of the
IL11
gene in IBD, two polymorphisms, including a dinucleotide repeat in the promoter region, have been genotyped in 222 patients with CD, 152 patients with ulcerative colitis (UC) and 400 healthy controls. PCR-SSCP analysis of the coding region revealed a single polymorphism in exon 4 leading to an amino acid exchange (G335A; R112H), not significantly associated with either disease. Dinucleotide repeat frequencies of the
IL11.A1
allele and of
IL11.A1
homozygous individuals were significantly increased among the patients with UC (
P
<0.002 and (
P
<0.003, respectively) but not with CD. Altered expression of
IL11
appears to be involved in the genetic predisposition of UC.</description><subject>Alleles</subject><subject>Amino acids</subject><subject>Antigens</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>brief-communication</subject><subject>Cancer Research</subject><subject>Colitis, Ulcerative - genetics</subject><subject>Crohn's disease</subject><subject>Dinucleotide Repeats - genetics</subject><subject>DNA binding proteins</subject><subject>Gene Expression</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Interleukin 1</subject><subject>Interleukin 11</subject><subject>Interleukin-11 - genetics</subject><subject>Leukocytes (mononuclear)</subject><subject>Lipopolysaccharides</subject><subject>NF-κB protein</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Promoter Regions, Genetic - immunology</subject><subject>Risk factors</subject><subject>Ulcerative colitis</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkttr2zAYxc1YWS_b896G2GCwB6eSLOvyGErXBQKFXZ6FIn9OFGwrk-Ru_e8nk0BIaRl6kJB-54gjnaJ4T_CM4Epex-1sDQPMeMUrqcSr4oIwwcuaCfx6WnNeMinUeXEZ4xZjwglXb4pzQpnkHKuL4naOdr577H3YbVzskRtQ2gBaLAlBkzNyEZkYvXUmQYP-uLRBY2chmOQeAFnfueTi2-KsNV2Ed4f5qvj19fbnzbdyeX-3uJkvS1tzlkqlWkEtU7TmrWI1tlwAwxzoqlopyYglK8CGVNw0ohUcGtaaupFZRWoCQlVXxee97y743yPEpHsXLXSdGcCPUQsqJK4x_i9IJJecEp7BT0_ArR_DkENoyhkRVNZqsvv4IkWkrDGt8NFqbTrQbmh9CsZO9-o5zW9PK1VNEWbPUHk00DvrB2hd3j8RfDkRZCbB37Q2Y4x68eP7KXu9Z23wMQZo9S643oRHTbCeCqPjVk_fqg-FyYoPh2TjqofmyB8akgG8B2I-GtYQjtFf8vwHESTHsQ</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Klein, W</creator><creator>Tromm, A</creator><creator>Griga, T</creator><creator>Fricke, H</creator><creator>Folwaczny, C</creator><creator>Hocke, M</creator><creator>Eitner, K</creator><creator>Marx, M</creator><creator>Duerig, N</creator><creator>Epplen, J T</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20021201</creationdate><title>A polymorphism in the IL11 gene is associated with ulcerative colitis</title><author>Klein, W ; Tromm, A ; Griga, T ; Fricke, H ; Folwaczny, C ; Hocke, M ; Eitner, K ; Marx, M ; Duerig, N ; Epplen, J T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-99f72c49256f9450c67e406e2b3b9841c1be0a136ad7f76ed4fa5d89f7151e793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Alleles</topic><topic>Amino acids</topic><topic>Antigens</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>brief-communication</topic><topic>Cancer Research</topic><topic>Colitis, Ulcerative - genetics</topic><topic>Crohn's disease</topic><topic>Dinucleotide Repeats - genetics</topic><topic>DNA binding proteins</topic><topic>Gene Expression</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genotype</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Interleukin 1</topic><topic>Interleukin 11</topic><topic>Interleukin-11 - genetics</topic><topic>Leukocytes (mononuclear)</topic><topic>Lipopolysaccharides</topic><topic>NF-κB protein</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Promoter Regions, Genetic - immunology</topic><topic>Risk factors</topic><topic>Ulcerative colitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klein, W</creatorcontrib><creatorcontrib>Tromm, A</creatorcontrib><creatorcontrib>Griga, T</creatorcontrib><creatorcontrib>Fricke, H</creatorcontrib><creatorcontrib>Folwaczny, C</creatorcontrib><creatorcontrib>Hocke, M</creatorcontrib><creatorcontrib>Eitner, K</creatorcontrib><creatorcontrib>Marx, M</creatorcontrib><creatorcontrib>Duerig, N</creatorcontrib><creatorcontrib>Epplen, J T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>AIDS and Cancer Research Abstracts</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>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><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klein, W</au><au>Tromm, A</au><au>Griga, T</au><au>Fricke, H</au><au>Folwaczny, C</au><au>Hocke, M</au><au>Eitner, K</au><au>Marx, M</au><au>Duerig, N</au><au>Epplen, J T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A polymorphism in the IL11 gene is associated with ulcerative colitis</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>3</volume><issue>8</issue><spage>494</spage><epage>496</epage><pages>494-496</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Inflammatory bowel diseases (IBD) are multifactorial disorders characterised by the host's inability to limit the inflammatory response to luminal antigens. The association of polymorphisms in the CARD15 gene with Crohn's disease (CD) demonstrates the relevance of activated transcription factor NF
κ
B in mononuclear cells. Interleukin 11 (IL11) mediates anti-inflammatory effects and is able to downregulate LPS-induced NF
κ
B activation. The
IL11
gene is therefore a good candidate involved in genetic predisposition to IBD. To evaluate the role of the
IL11
gene in IBD, two polymorphisms, including a dinucleotide repeat in the promoter region, have been genotyped in 222 patients with CD, 152 patients with ulcerative colitis (UC) and 400 healthy controls. PCR-SSCP analysis of the coding region revealed a single polymorphism in exon 4 leading to an amino acid exchange (G335A; R112H), not significantly associated with either disease. Dinucleotide repeat frequencies of the
IL11.A1
allele and of
IL11.A1
homozygous individuals were significantly increased among the patients with UC (
P
<0.002 and (
P
<0.003, respectively) but not with CD. Altered expression of
IL11
appears to be involved in the genetic predisposition of UC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12486609</pmid><doi>10.1038/sj.gene.6363897</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alleles Amino acids Antigens Biomedical and Life Sciences Biomedicine brief-communication Cancer Research Colitis, Ulcerative - genetics Crohn's disease Dinucleotide Repeats - genetics DNA binding proteins Gene Expression Gene polymorphism Genetic aspects Genetic polymorphisms Genotype Health aspects Human Genetics Humans Immunology Inflammatory bowel disease Inflammatory bowel diseases Interleukin 1 Interleukin 11 Interleukin-11 - genetics Leukocytes (mononuclear) Lipopolysaccharides NF-κB protein Physiological aspects Polymorphism Polymorphism, Genetic Polymorphism, Single-Stranded Conformational Promoter Regions, Genetic - immunology Risk factors Ulcerative colitis |
title | A polymorphism in the IL11 gene is associated with ulcerative colitis |
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