| dc.contributor.author |
Gazouli, M |
en |
| dc.contributor.author |
Mantzaris, G |
en |
| dc.contributor.author |
Kotsinas, A |
en |
| dc.contributor.author |
Zacharatos, P |
en |
| dc.contributor.author |
Papalambros, E |
en |
| dc.contributor.author |
Archimandritis, A |
en |
| dc.contributor.author |
Ikonomopoulos, J |
en |
| dc.contributor.author |
Gorgoulis, VG |
en |
| dc.date.accessioned |
2014-06-06T06:46:26Z |
|
| dc.date.available |
2014-06-06T06:46:26Z |
|
| dc.date.issued |
2005 |
en |
| dc.identifier.issn |
10079327 |
en |
| dc.identifier.uri |
http://62.217.125.90/xmlui/handle/123456789/3006 |
|
| dc.relation.uri |
http://www.scopus.com/inward/record.url?eid=2-s2.0-13544276471&partnerID=40&md5=3206e32f584b78885be138ab3953ace7 |
en |
| dc.subject |
CARD15/NOD2 gene |
en |
| dc.subject |
CD14 antigen |
en |
| dc.subject |
Inflamatory bowel disease |
en |
| dc.subject |
Toll-like receptor 4 |
en |
| dc.subject.other |
caspase recruitment domain protein 15 |
en |
| dc.subject.other |
CD14 antigen |
en |
| dc.subject.other |
toll like receptor |
en |
| dc.subject.other |
allele |
en |
| dc.subject.other |
article |
en |
| dc.subject.other |
blood sampling |
en |
| dc.subject.other |
controlled study |
en |
| dc.subject.other |
Crohn disease |
en |
| dc.subject.other |
DNA isolation |
en |
| dc.subject.other |
drug disposition |
en |
| dc.subject.other |
gene |
en |
| dc.subject.other |
gene interaction |
en |
| dc.subject.other |
gene mutation |
en |
| dc.subject.other |
genetic polymorphism |
en |
| dc.subject.other |
genetic susceptibility |
en |
| dc.subject.other |
genetic variability |
en |
| dc.subject.other |
genotype |
en |
| dc.subject.other |
Greece |
en |
| dc.subject.other |
human |
en |
| dc.subject.other |
human cell |
en |
| dc.subject.other |
innate immunity |
en |
| dc.subject.other |
major clinical study |
en |
| dc.subject.other |
multifactorial genetic disorder |
en |
| dc.subject.other |
pathogenesis |
en |
| dc.subject.other |
promoter region |
en |
| dc.subject.other |
risk factor |
en |
| dc.subject.other |
ulcerative colitis |
en |
| dc.subject.other |
Antigens, CD14 |
en |
| dc.subject.other |
Colitis, Ulcerative |
en |
| dc.subject.other |
Crohn Disease |
en |
| dc.subject.other |
Female |
en |
| dc.subject.other |
Gene Frequency |
en |
| dc.subject.other |
Genetic Predisposition to Disease |
en |
| dc.subject.other |
Genotype |
en |
| dc.subject.other |
Greece |
en |
| dc.subject.other |
Humans |
en |
| dc.subject.other |
Intracellular Signaling Peptides and Proteins |
en |
| dc.subject.other |
Male |
en |
| dc.subject.other |
Membrane Glycoproteins |
en |
| dc.subject.other |
Nod2 Signaling Adaptor Protein |
en |
| dc.subject.other |
Polymorphism, Genetic |
en |
| dc.subject.other |
Promoter Regions (Genetics) |
en |
| dc.subject.other |
Receptors, Cell Surface |
en |
| dc.subject.other |
Risk Factors |
en |
| dc.subject.other |
Toll-Like Receptor 4 |
en |
| dc.subject.other |
Toll-Like Receptors |
en |
| dc.title |
Association between polymorphisms in the Toll-like receptor 4, CD14, and CARD15/NOD2 and inflammatory bowel disease in the Greek population |
en |
| heal.type |
journalArticle |
en |
| heal.publicationDate |
2005 |
en |
| heal.abstract |
Aim: Crohn's disease (CD) and ulcerative colitis (UC) are multifactorial diseases with a significant genetic background. Apart from CARD15/NOD2 gene, evidence is accumulating that molecules related to the innate immune response such as CD14 or Toll-like receptor 4 (TLR4), are involved in their pathogenesis. In further exploring the genetic background of these diseases, we investigated the variations in the CARD15/NOD2 gene (Arg702Trp, Gly908Arg and Leu1007fsinsC), and polymorphisms in the TLR4 gene (Asp299Gly and Thr399Ile) as well as in the promoter of the CD14 gene (T/C at position -159) in Greek patients with CD and UC. Methods: DNA was obtained from 120 patients with CD, 85 with UC and 100 healthy individuals. Genotyping was performed by allele specific PCR or by PCR-RFLP analysis. Results: The 299Gly allele frequency of the TLR4 gene and the T allele and TT genotype frequencies of the CD14 promoter were significantly higher in CD patients only compared to healthy individuals (P = 0.026<0.05; P = 0.0048<0.01 and P = 0.047<0.05 respectively). Concerning the NOD2/CARD15 mutations the overall presence in CD patients was significantly higher than that in UC patients or in controls. Additionally, 51.67% of the CD patients were carriers of a TLR4 and/or CD14 polymorphic allele and at least one variant of the NOD2/CARD15, compared to 27% of the UC patients. It should be pointed out that both frequencies significantly increased as compared with the 10% frequency of multiple carriers found in healthy controls. A possible interaction of the NOD2/CARD15 with TLR4 and especially CD14, increased the risk of developing inflammatory bowel disease (IBD). Conclusion: Our results indicate that co-existence of a mutation in either the TLR4 or CD14 gene, and in NOD2/CARD15 is associated with an increased susceptibility to developing CD compared to UC, and to developing either CD or UC compared to healthy individuals. © 2005 The WJG Press and Elsevier Inc. All rights reserved. |
en |
| heal.journalName |
World Journal of Gastroenterology |
en |
| dc.identifier.issue |
5 |
en |
| dc.identifier.volume |
11 |
en |
| dc.identifier.spage |
681 |
en |
| dc.identifier.epage |
685 |
en |