Abstract
Background and Aims: Celiac disease is a chronic inflammatory disease of the intestines that occurs after gluten intake in genetically susceptible individuals. The intercellular adhesion molecule -1 gene codes for the intercellular adhesion molecule -1protein, which plays a pivotal role in inflammatory diseases. intercellular adhesion molecule -1 levels have been shown to be increased in celiac disease patients. We aimed to define the relationship between an intercellular adhesion molecule -1 gene polymorphism and celiac disease risk in the Turkish population. Material and Methods: Forty celiac disease patients and 40 healthy controls were included in this study. The G241 R (rs 1799969) polymorphism was analyzed. Results: No statistically significant difference was detected in the frequency of the G241R polymorphism in the intercellular adhesion molecule -1 gene between celiac disease patients and healthy controls. Discussion: Further larger scale analyses are needed to support the findings of the present study.
References
- 1. Ferguson A, MacDonald TT, McClure JP, Holden RJ. Cell-mediated immunity to gliadin within the small-intestinal mucosa in coeliac disease. Lancet 1975;1:895-7. 2. Sollid LM. Coeliac disease: dissecting a complex inflammatory disorder. Nat Rev Immunol 2002;2:647-55. 3. Sollid LM, Markussen G, Ek J, et al. Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer. J Exp Med 1989;169:345-50. 4. Monsuur AJ, de Bakker PI, Alizadeh BZ, et al. Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect. Nat Genet 2005;37:1341-4. 5. Curley CR, Monsuur AJ, Wapenaar MC, et al. A functional candidate screen for coeliac disease genes. Eur J Hum Genet 2006;14:1215-22. 6. van de Stolpe A, van der Saag PT. Intercellular adhesion molecule-1. J Mol Med (Berl) 1996;74:13-33. 7. Sturgess RP, Macartney JC, Makgoba MW, et al. Differential upregulation of intercellular adhesion molecule-1 in coeliac disease. Clin Exp Immunol 1990;82:489-92. 8. Jelínková L, Tucková L, Sánchez D, et al. Increased levels of circulating ICAM-1, E-selectin, and IL-2 receptors in celiac disease. Dig Dis Sci 2000;45:398-402. 9. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Revised criteria for diagnosis of coeliac disease. Arch Dis Child 1990;65:909-11. 10. Abel M, Cellier C, Kumar N, Cerf-Bensussan N, et al. Hum adulthood-onset celiac disease is associated with intercellular adhesion molecule-1 (ICAM-1) gene polymorphism. Immunol 2006;67:612-7. 11. Kaur G, Rapthap CC, Kumar S, et al. Polymorphism in L-selectin, E-selectin and ICAM-1 genes in Asian Indian pediatric patients with celiac disease. Hum Immunol 2006;67:634-8. 12. Dema B, Martínez A, Polanco I, et al. ICAM1 R241 is not associated with celiac disease in the Spanish population. Hum Immunol 2008;69:675-8.
Abstract
Giriş ve Amaç: Çölyak hastalığı, genetik olarak yatkın kişilerde gluten alımından sonra gelişen kronik intestinal inflamatuvar hastalıktır. İntersellüler adezyon molekül-1 geni, inflamatuvar olaylarda rol alan intersellüler adezyon molekül-1’i kodlamaktadır. Çölyak hastalığı olanların intestinal biyopsi ve serumlarında intersellüler adezyon molekül-1 seviyelerinde artış gösterilmiştir. Bu çalışmada amacımız, çölyak hastalığı riski ile intersellüler adezyon molekül-1 gen polimorfizminin ilişkisini araştırmaktı. Gereç ve Yöntem: Çalışmaya 40 çölyak hastası ve 40 sağlıklı kontrol dahil edildi. İntersellüler adezyon molekül-1 genindeki G241R(rs1799969) polimorfizmi analiz edildi. Bulgular: Çölyak hastalığı olanlarla kontrol grubu arasında intersellüler adezyon molekül-1 geninde G241R polimorfizmi yönünden istatistiksel olarak anlamlı fark saptamadık. Sonuç: Bizim çalışmamızdaki sonuçlara göre çölyak hastalığında intersellüler adezyon molekül-1 G241’in rolünü gösteremedik.
References
- 1. Ferguson A, MacDonald TT, McClure JP, Holden RJ. Cell-mediated immunity to gliadin within the small-intestinal mucosa in coeliac disease. Lancet 1975;1:895-7. 2. Sollid LM. Coeliac disease: dissecting a complex inflammatory disorder. Nat Rev Immunol 2002;2:647-55. 3. Sollid LM, Markussen G, Ek J, et al. Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer. J Exp Med 1989;169:345-50. 4. Monsuur AJ, de Bakker PI, Alizadeh BZ, et al. Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect. Nat Genet 2005;37:1341-4. 5. Curley CR, Monsuur AJ, Wapenaar MC, et al. A functional candidate screen for coeliac disease genes. Eur J Hum Genet 2006;14:1215-22. 6. van de Stolpe A, van der Saag PT. Intercellular adhesion molecule-1. J Mol Med (Berl) 1996;74:13-33. 7. Sturgess RP, Macartney JC, Makgoba MW, et al. Differential upregulation of intercellular adhesion molecule-1 in coeliac disease. Clin Exp Immunol 1990;82:489-92. 8. Jelínková L, Tucková L, Sánchez D, et al. Increased levels of circulating ICAM-1, E-selectin, and IL-2 receptors in celiac disease. Dig Dis Sci 2000;45:398-402. 9. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Revised criteria for diagnosis of coeliac disease. Arch Dis Child 1990;65:909-11. 10. Abel M, Cellier C, Kumar N, Cerf-Bensussan N, et al. Hum adulthood-onset celiac disease is associated with intercellular adhesion molecule-1 (ICAM-1) gene polymorphism. Immunol 2006;67:612-7. 11. Kaur G, Rapthap CC, Kumar S, et al. Polymorphism in L-selectin, E-selectin and ICAM-1 genes in Asian Indian pediatric patients with celiac disease. Hum Immunol 2006;67:634-8. 12. Dema B, Martínez A, Polanco I, et al. ICAM1 R241 is not associated with celiac disease in the Spanish population. Hum Immunol 2008;69:675-8.
Details
| Subjects | Health Care Administration |
|---|---|
| Journal Section | Articles |
| Authors | |
| Publication Date | April 24, 2017 |
| Published in Issue | Year 2017 Volume: 16 Issue: 1 |
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