Journal
CLINICAL IMMUNOLOGY
Volume 127, Issue 1, Pages 49-55Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2007.11.016
Keywords
Crohn's disease; ulcerative colitis; inflammatory bowel; disease; chemokine; CXCL1 6; CXCR6; polymorphism; genetics; intestinal inflammation; CARD15
Categories
Funding
- NIDDK NIH HHS [R01 DK068181, P01 DK003506] Funding Source: Medline
Ask authors/readers for more resources
To identify if genetic determinants of CXCL16 modulate the susceptibility and phenotype of inflammatory bowel diseases (IBD), we analyzed genomic DNA from 574 individuats (365 IBD patients, 209 healthy controls) for the CXCL16 p.Ala181Va1 polymorphism. In this study, we demonstrate that in Crohn's disease (CD), the CXCL16 p.ALa181Val polymorphism is not a disease susceptibility gene but associated with younger age at disease onset (p=0.016) and higher frequency of ilea( involvement (p=0.024; OR 2.17; 95% CI 1.12-4.21) in ValVal carriers compared to a higher frequency of colonic involvement in AlaAla carriers (p = 0.009; OR 2.60; CI 1.29-5.25). Carriers of at least one Val allele and one CARD15/NOD2 variant had a higher incidence of a stricturing and penetrating phenotype (p = 0.030, OR 4.04, CI 1.27-12.84) and of stenoses (p = 0.014; OR 3.97; Cl 1.38-11.40) than patients carrying NOD2 variants only, suggesting that this polymorphism contributes to a severe disease phenotype in CD. (C) 2007 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available