Author/Authors :
Seiderer، نويسنده , , Julia and Dambacher، نويسنده , , Julia and Leistner، نويسنده , , Dorothea and Tillack، نويسنده , , Cornelia and Glas، نويسنده , , Jürgen and Niess، نويسنده , , Jan-Hendrik and Pfennig، نويسنده , , Simone and Jürgens، نويسنده , , Matthias and Müller-Myhsok، نويسنده , , Bertram and Gِke، نويسنده , , Burkhard and Ochsenkühn، نويسنده , , Thomas and Lohse-Busch، نويسنده , , Peter and R، نويسنده ,
Abstract :
To identify if genetic determinants of CXCL16 modulate the susceptibility and phenotype of inflammatory bowel diseases (IBD), we analyzed genomic DNA from 574 individuals (365 IBD patients, 209 healthy controls) for the CXCL16 p.Ala181Val polymorphism. In this study, we demonstrate that in Crohnʹs 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 ileal 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; CI 1.38–11.40) than patients carrying NOD2 variants only, suggesting that this polymorphism contributes to a severe disease phenotype in CD.
Keywords :
inflammatory bowel disease , Chemokine , CXCL16 , CXCR6 , Polymorphism , genetics , Intestinal inflammation , CARD15 , Crohnיs disease , ulcerative colitis
