Fractalkine receptor polymorphism may not be associated with the development and clinical course of ulcerative colitis

• Published in: Bosnian journal of basic medical sciences Vol. 15; no. 2; pp. 73 - 77
• Main Authors: Gokcan, Hale, Yurtcu, Erkan, Selcuk, Haldun, Sahin, Feride I
• Format: Journal Article
• Language: English
• Published: Bosnia and Herzegovina Association of Basic Medical Sciences 01.05.2015; Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina
• Subjects: Adult; Analysis; Case-Control Studies; Colitis, Ulcerative - genetics; CX3C Chemokine Receptor 1; Female; Gene Frequency - genetics; Genetic Predisposition to Disease - genetics; Genotype; Humans; Male; Middle Aged; Phenotype; Polymerase chain reaction; Polymorphism, Single Nucleotide - genetics; Receptors, Chemokine - genetics; Risk Factors; Single nucleotide polymorphisms; Ulcerative colitis
• ISSN: 1512-8601; 1840-4812
• DOI: 10.17305/bjbms.2015.387

Fractalkine (CX3C), a chemokine expressed by epithelial cells within normal and inflamed colorectal mucosa, induces leukocyte adhesion and migration via fractalkine receptor. The aim of this study was to investigate two single nucleotide polymorphisms of the fractalkine receptor gene as a risk factor both for the development and clinical findings of ulcerative colitis. In this study, 51 patients with ulcerative colitis (UC) and 80 controls were recruited. Genotypes of fractalkine receptorc.745G>A (V249I) and c.839C>T (T280M) polymorphisms were identified by restriction fragment length polymorphism analyses after polymerase chain reaction.Genotype distribution and allele frequencies of V249I and T280M were not statistically significantly different between UC and control groups (p>0.05). No statistically significant relationship was found between fractalkine receptor polymorphisms and clinical findings of UC. We observed no significant difference in fractalkine receptor polymorphism between patients and control group and no genotype-phenotype relation. Therefore, we concluded that fractalkine receptor polymorphisms may not contribute to the molecular pathogenesis of UC.