Lack of association of the CD14 promoter polymorphism −159C/T with Caucasian inflammatory bowel disease
Objective The inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial diseases resulting from a complex interaction of genetic and environmental factors. The recently described CARD15 and TNF-α risk alleles are believed to be contributo...
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| Veröffentlicht in: | Scandinavian journal of gastroenterology 2005-02, Vol.40 (2), p.194-197 |
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| container_title | Scandinavian journal of gastroenterology |
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| creator | Peters, Kirsten E. O'Callaghan, Nathan J. Cavanaugh, Juleen A. |
| description | Objective
The inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial diseases resulting from a complex interaction of genetic and environmental factors. The recently described CARD15 and TNF-α risk alleles are believed to be contributors to disease by disrupting inflammatory pathways via impaired response to bacteria. Other bacterial receptors, such as CD14, may also have a role in disease. A promoter polymorphism (−159C/T) in CD14 has been implicated in IBD in a number of studies.
Material and methods
We have analysed this CD14 promoter polymorphism in probands from 206 multiplex IBD families, 110 sporadic IBD individuals and 189 healthy controls from the Australian population, all of whom are Caucasian.
Results
We could not replicate the described association between the CD14-159T allele and CD or UC, nor did we find any evidence for an interaction between the CARD15 or TNF-α risk alleles and the CD14-159T allele.
Conclusions
It is possible that the association seen in other studies may be due to population stratification or to the CD14 polymorphism being in linkage with the real disease-causing variant(s). |
| doi_str_mv | 10.1080/00365520510011506 |
| format | Article |
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The inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial diseases resulting from a complex interaction of genetic and environmental factors. The recently described CARD15 and TNF-α risk alleles are believed to be contributors to disease by disrupting inflammatory pathways via impaired response to bacteria. Other bacterial receptors, such as CD14, may also have a role in disease. A promoter polymorphism (−159C/T) in CD14 has been implicated in IBD in a number of studies.
Material and methods
We have analysed this CD14 promoter polymorphism in probands from 206 multiplex IBD families, 110 sporadic IBD individuals and 189 healthy controls from the Australian population, all of whom are Caucasian.
Results
We could not replicate the described association between the CD14-159T allele and CD or UC, nor did we find any evidence for an interaction between the CARD15 or TNF-α risk alleles and the CD14-159T allele.
Conclusions
It is possible that the association seen in other studies may be due to population stratification or to the CD14 polymorphism being in linkage with the real disease-causing variant(s).</description><identifier>ISSN: 0036-5521</identifier><identifier>EISSN: 1502-7708</identifier><identifier>DOI: 10.1080/00365520510011506</identifier><identifier>PMID: 15764151</identifier><identifier>CODEN: SJGRA4</identifier><language>eng</language><publisher>Copenhagen: Informa UK Ltd</publisher><subject>Australia ; Biological and medical sciences ; CARD15 ; CD14 ; European Continental Ancestry Group - genetics ; Gastroenterology. Liver. Pancreas. Abdomen ; Genetic Predisposition to Disease ; Genotype ; Humans ; IBD ; Inflammatory Bowel Diseases - genetics ; Intracellular Signaling Peptides and Proteins - genetics ; Lipopolysaccharide Receptors - genetics ; Medical sciences ; NOD2 ; Nod2 Signaling Adaptor Protein ; Other diseases. Semiology ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumor Necrosis Factor-alpha</subject><ispartof>Scandinavian journal of gastroenterology, 2005-02, Vol.40 (2), p.194-197</ispartof><rights>2005 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2005</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-5ffa5af4bcc63c87b5c8652a4abdae881c9c77bf8aa120b2ef440df3f911fc163</citedby><cites>FETCH-LOGICAL-c434t-5ffa5af4bcc63c87b5c8652a4abdae881c9c77bf8aa120b2ef440df3f911fc163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/00365520510011506$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/00365520510011506$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,59647,59753,60436,60542,61221,61256,61402,61437</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16459983$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15764151$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peters, Kirsten E.</creatorcontrib><creatorcontrib>O'Callaghan, Nathan J.</creatorcontrib><creatorcontrib>Cavanaugh, Juleen A.</creatorcontrib><title>Lack of association of the CD14 promoter polymorphism −159C/T with Caucasian inflammatory bowel disease</title><title>Scandinavian journal of gastroenterology</title><addtitle>Scand J Gastroenterol</addtitle><description>Objective
The inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial diseases resulting from a complex interaction of genetic and environmental factors. The recently described CARD15 and TNF-α risk alleles are believed to be contributors to disease by disrupting inflammatory pathways via impaired response to bacteria. Other bacterial receptors, such as CD14, may also have a role in disease. A promoter polymorphism (−159C/T) in CD14 has been implicated in IBD in a number of studies.
Material and methods
We have analysed this CD14 promoter polymorphism in probands from 206 multiplex IBD families, 110 sporadic IBD individuals and 189 healthy controls from the Australian population, all of whom are Caucasian.
Results
We could not replicate the described association between the CD14-159T allele and CD or UC, nor did we find any evidence for an interaction between the CARD15 or TNF-α risk alleles and the CD14-159T allele.
Conclusions
It is possible that the association seen in other studies may be due to population stratification or to the CD14 polymorphism being in linkage with the real disease-causing variant(s).</description><subject>Australia</subject><subject>Biological and medical sciences</subject><subject>CARD15</subject><subject>CD14</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>IBD</subject><subject>Inflammatory Bowel Diseases - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Lipopolysaccharide Receptors - genetics</subject><subject>Medical sciences</subject><subject>NOD2</subject><subject>Nod2 Signaling Adaptor Protein</subject><subject>Other diseases. Semiology</subject><subject>Polymorphism, Genetic</subject><subject>Promoter Regions, Genetic</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumor Necrosis Factor-alpha</subject><issn>0036-5521</issn><issn>1502-7708</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM-KFDEQh4Mo7uzqA3iRXPTWbqo76T_oRVpXhQEv67mpTid01qQzJmmGeQPPPqJPYoYZWUTYU1HU9yuqPkJeAHsDrGXXjFW1ECUTwBiAYPUjssmlLJqGtY_J5jgvMgAX5DLGO8aYaHj3lFyAaGoOAjbEbFF-p15TjNFLg8n45dimWdH-A3C6C975pALdeXtwPuxmEx39_fMXiK6_vqV7k2ba4yoxGlyoWbRF5zD5cKCj3ytLJxMVRvWMPNFoo3p-rlfk283H2_5zsf366Uv_fltIXvFUCK1RoOajlHUl22YUsq1FiRzHCVXbguxk04y6RYSSjaXSnLNJV7oD0BLq6oq8Pu3Nl_9YVUyDM1Eqa3FRfo1D3Rx1dU0G4QTK4GMMSg-7YByGwwBsOPod_vObMy_Py9fRqek-cRaagVdnAKNEqwMu0sR7ruai69oqc-9OXBbmg8O9D3YaEh6sD39D1UN3vP0nPiu0aZYY1HDn17BkwQ988QfiIKkP</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Peters, Kirsten E.</creator><creator>O'Callaghan, Nathan J.</creator><creator>Cavanaugh, Juleen A.</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><general>Scandinavian University Press</general><scope>IQODW</scope><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></search><sort><creationdate>20050201</creationdate><title>Lack of association of the CD14 promoter polymorphism −159C/T with Caucasian inflammatory bowel disease</title><author>Peters, Kirsten E. ; O'Callaghan, Nathan J. ; Cavanaugh, Juleen A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-5ffa5af4bcc63c87b5c8652a4abdae881c9c77bf8aa120b2ef440df3f911fc163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Australia</topic><topic>Biological and medical sciences</topic><topic>CARD15</topic><topic>CD14</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>IBD</topic><topic>Inflammatory Bowel Diseases - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Lipopolysaccharide Receptors - genetics</topic><topic>Medical sciences</topic><topic>NOD2</topic><topic>Nod2 Signaling Adaptor Protein</topic><topic>Other diseases. Semiology</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumor Necrosis Factor-alpha</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peters, Kirsten E.</creatorcontrib><creatorcontrib>O'Callaghan, Nathan J.</creatorcontrib><creatorcontrib>Cavanaugh, Juleen A.</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Scandinavian journal of gastroenterology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peters, Kirsten E.</au><au>O'Callaghan, Nathan J.</au><au>Cavanaugh, Juleen A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of association of the CD14 promoter polymorphism −159C/T with Caucasian inflammatory bowel disease</atitle><jtitle>Scandinavian journal of gastroenterology</jtitle><addtitle>Scand J Gastroenterol</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>40</volume><issue>2</issue><spage>194</spage><epage>197</epage><pages>194-197</pages><issn>0036-5521</issn><eissn>1502-7708</eissn><coden>SJGRA4</coden><abstract>Objective
The inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial diseases resulting from a complex interaction of genetic and environmental factors. The recently described CARD15 and TNF-α risk alleles are believed to be contributors to disease by disrupting inflammatory pathways via impaired response to bacteria. Other bacterial receptors, such as CD14, may also have a role in disease. A promoter polymorphism (−159C/T) in CD14 has been implicated in IBD in a number of studies.
Material and methods
We have analysed this CD14 promoter polymorphism in probands from 206 multiplex IBD families, 110 sporadic IBD individuals and 189 healthy controls from the Australian population, all of whom are Caucasian.
Results
We could not replicate the described association between the CD14-159T allele and CD or UC, nor did we find any evidence for an interaction between the CARD15 or TNF-α risk alleles and the CD14-159T allele.
Conclusions
It is possible that the association seen in other studies may be due to population stratification or to the CD14 polymorphism being in linkage with the real disease-causing variant(s).</abstract><cop>Copenhagen</cop><cop>Oslo</cop><cop>Stockholm</cop><pub>Informa UK Ltd</pub><pmid>15764151</pmid><doi>10.1080/00365520510011506</doi><tpages>4</tpages></addata></record> |
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| ispartof | Scandinavian journal of gastroenterology, 2005-02, Vol.40 (2), p.194-197 |
| issn | 0036-5521 1502-7708 |
| language | eng |
| recordid | cdi_pascalfrancis_primary_16459983 |
| source | MEDLINE; Taylor & Francis:Master (3349 titles); Taylor & Francis Medical Library - CRKN |
| subjects | Australia Biological and medical sciences CARD15 CD14 European Continental Ancestry Group - genetics Gastroenterology. Liver. Pancreas. Abdomen Genetic Predisposition to Disease Genotype Humans IBD Inflammatory Bowel Diseases - genetics Intracellular Signaling Peptides and Proteins - genetics Lipopolysaccharide Receptors - genetics Medical sciences NOD2 Nod2 Signaling Adaptor Protein Other diseases. Semiology Polymorphism, Genetic Promoter Regions, Genetic Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumor Necrosis Factor-alpha |
| title | Lack of association of the CD14 promoter polymorphism −159C/T with Caucasian inflammatory bowel disease |
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