Publication: Association between bactericidal/permeability increasing protein (BPI) gene polymorphism (Lys216Glu) and inflammatory bowel disease
| dc.contributor.author | EREN, FATİH | |
| dc.contributor.authors | Akin, Hakan; Tahan, Gulgun; Ture, Filiz; Eren, Fatih; Atug, Ozlen; Tahan, Veysel; Hamzaoglu, Ismail; Imeryuz, Nese; Tozun, Nurdan; Hamzaoglu, Hulya Over | |
| dc.date.accessioned | 2022-03-14T09:51:34Z | |
| dc.date.available | 2022-03-14T09:51:34Z | |
| dc.date.issued | 2011-02 | |
| dc.description.abstract | Background: Increasing Increasing evidence suggests that innate immune system may have a key role in the pathogenesis of the inflammatory bowel disease (IBD). Bactericidal/permeability increasing protein (BPI) has an important role in the recognition and neutralization of gram-negative bacteria by host innate immune system. The polymorphism on BPI gene called Lys216Glu is on the suspected list of IBD pathogenesis. Methods: We studied the Lys216Glu polymorphism on BPI gene, in a Turkish IBD patient population. A total of 238 IBD patients; 116 Crohn's disease (CD) and 122 ulcerative colitis (UC), besides 197 healthy controls were included in this study. Results: The Glu/Glu genotype and allele frequencies were found to be statistically higher compared to healthy control group not only in CD patients [P: 0.03, OR: 1.87 (CI 95% 1.02-3.42) and P: 0.00001 (OR: 2.07 CI 95% 1.47-2.91) respectively] but also in UC patients [P: 0.0002, OR: 2.71 (CI 95% 1.53-4.80) and P: 0.00002 (OR: 2.71 CI 95% 1.53-4.80) respectively]. Conclusions: BPI polymorphism (Lys216Glu) is associated both to CD and UC. Our findings differ from the two Western European studies; one without any association and the other indicating an association only with CD. Our study is the first one reporting a novel association between BPI gene mutation (Lys216Glu) and UC. (C) 2010 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved. | |
| dc.identifier.doi | 10.1016/j.crohns.2010.08.008 | |
| dc.identifier.issn | 1873-9946 | |
| dc.identifier.pubmed | 21272798 | |
| dc.identifier.uri | https://hdl.handle.net/11424/243348 | |
| dc.identifier.wos | WOS:000288822300003 | |
| dc.language.iso | eng | |
| dc.publisher | ELSEVIER SCIENCE BV | |
| dc.relation.ispartof | JOURNAL OF CROHNS & COLITIS | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | Inflammatory bowel disease | |
| dc.subject | Bactericidal/permeability increasing protein | |
| dc.subject | Pathogenesis | |
| dc.subject | Polymorphism | |
| dc.subject | ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES | |
| dc.subject | CROHNS-DISEASE | |
| dc.subject | ULCERATIVE-COLITIS | |
| dc.subject | INNATE IMMUNITY | |
| dc.subject | VARIANTS | |
| dc.subject | MUTATION | |
| dc.subject | TOLL | |
| dc.subject | AUTOANTIBODIES | |
| dc.subject | SUSCEPTIBILITY | |
| dc.subject | PATHOGENESIS | |
| dc.title | Association between bactericidal/permeability increasing protein (BPI) gene polymorphism (Lys216Glu) and inflammatory bowel disease | |
| dc.type | article | |
| dspace.entity.type | Publication | |
| local.avesis.id | 30520fbe-0c94-487e-a432-28d085de90d0 | |
| local.import.package | SS16 | |
| local.indexed.at | WOS | |
| local.indexed.at | SCOPUS | |
| local.indexed.at | PUBMED | |
| local.journal.numberofpages | 5 | |
| oaire.citation.endPage | 18 | |
| oaire.citation.issue | 1 | |
| oaire.citation.startPage | 14 | |
| oaire.citation.title | JOURNAL OF CROHNS & COLITIS | |
| oaire.citation.volume | 5 | |
| relation.isAuthorOfPublication | 4bc77d63-5aa7-4c67-8d60-12778ea963b1 | |
| relation.isAuthorOfPublication.latestForDiscovery | 4bc77d63-5aa7-4c67-8d60-12778ea963b1 |
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