IL23R and ATG16L1 variants in Moroccan patients with inflammatory bowel disease

BMC Research Notes

Sellama Nadifi²  Wafaa Badre¹  Brehima Diakite²  Nezha Senhaji²  Nadia Serbati² 

[1] Department of Gastro-enterology, CHU IBN ROCHD, Casablanca, Morocco;University Ain Chock Hassan Ii, Center Of Doctoral Sciences “In Health Sciences”, Casablanca, Morocco

关键词: Moroccan population;    IL23R;    ATG16L1;    IBD;   

Others  :  1130160
DOI  :  10.1186/1756-0500-7-570

 received in 2014-04-24, accepted in 2014-08-14,  发布年份 2014

【 摘 要 】

Background

Inflammatory bowel diseases (IBD) are chronic diseases of the gastrointestinal tract. Although their pathogenesis is unclear, the combination of genetic predisposition and environmental components are believed to be the main cause of these diseases. Recently, many variants in interleukin 23 receptor (IL23R) and autophagy-related 16-like 1 (ATG16L1) genes have been associated with the disease. Our objective was to assess the frequency of ATG16L1 (T300A) and IL23R (L310P) variants in Moroccan IBD (Crohn’s disease and Ulcerative Colitis) patients and to evaluate a possible effect of these variants on disease’s phenotype and clinical course.

Methods

96 Moroccan IBD patients and 114 unrelated volunteers were genotyped for ATG16L1 (T300A) and IL23R (L310P) variants by PCR-restriction fragment length polymorphism.

Results

This is the first report on the prevalence of ATG16L1 (T300A) and IL23R (L310P) variants in a Moroccan group. We found that IL23R (L310P) variant conferred a protective effect for crohn’s disease (CD) but not ulcerative colitis (UC) patients. The presence of ATG16L1 (T300A) mutated alleles was associated with CD type but not with disease onset. In addition, the carriage of T300A variant alleles conferred a protective effect in UC.

Conclusion

Our results showed that the prevalence of ATG16L1 and IL23R variants was not significantly different between patients and controls. However a possible role of ATG16L1 (T300A) on CD phenotype was suggested.

【 授权许可】

   
2014 Serbati et al.; licensee BioMed Central Ltd.

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