Research Article Genetic Polymorphisms of Multidrug Resistance Gene-1 (MDR1/ABCB1) and Glutathione S-Transferase Gene and the Risk of Inflammatory Bowel Disease among Moroccan Patients Nezha Senhaji, 1 Yaya Kassogue, 1 Mina Fahimi, 2 Nadia Serbati, 1 Wafaa Badre, 2 and Sellama Nadifi 1 1 Laboratory of Genetics and Molecular Pathologies, Faculty of Medicine and Pharmacy of Casablanca, Casablanca, Morocco 2 Gastroenterology Department, CHU Ibn Rochd, Casablanca, Morocco Correspondence should be addressed to Sellama Nadif; nadif@labgenmed.com Received 29 May 2015; Revised 6 September 2015; Accepted 8 September 2015 Academic Editor: Tˆ ania Silvia Fr¨ ode Copyright © 2015 Nezha Senhaji et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Infammatory bowel diseases (IBD) are multifactorial disorders resulting from environmental and genetic factors. Polymorphisms in MDR1 and GSTs genes might explain individual diferences in susceptibility to IBD. We carried out a case-control study to examine the association of MDR1 (C1236T and C3435T), GSTT1, and GSTM1 polymorphisms with the risk of IBD. Subjects were genotyped using PCR-RFLP for MDR1 gene and multiplex PCR for GSTT1 and GSTM1. Meta-analysis was performed to test the association of variant allele carriage with IBD risk. We report that GSTT1 null genotype is signifcantly associated with the risk of CD (OR: 2.5, CI: 1.2–5,  = 0.013) and UC (OR: 3.5, CI: 1.5–8.5,  = 0.004) and can infuence Crohn’s disease behavior. Te interaction between GSTT1 and GSTM1 genes showed that the combined null genotypes were associated with the risk of UC (OR: 3.1, CI: 1.1–9,  = 0.049). Furthermore, when compared to combined 1236CC/CT genotypes, the 1236TT genotype of MDR1 gene was associated with the risk of UC (OR: 3.7, CI: 1.3–10.7,  = 0.03). Meta-analysis demonstrated signifcantly higher frequencies of 3435T carriage in IBD patients. Our results show that GSTT1 null and MDR1 polymorphisms could play a role in susceptibility to IBD. 1. Introduction Infammatory bowel disease (IBD) is a multifactorial disorder of the gastrointestinal tract including Crohn’s disease (CD) and ulcerative colitis (UC). Although considerable progress has been made in the feld of IBD research, the under- lying etiopathogenesis is still under investigation [1]. It is assumed that inappropriate immune response to commensal intestinal bacteria associated with defective mucosal barrier related to genetic and environmental factors might play a fundamental role in the onset of IBD [2, 3]. Te involve- ment of oxidant/antioxidant imbalance in the development and severity of IBD is well documented. Previous studies have demonstrated the role of candidate genes such as the multidrug resistance 1 (MDR1) and glutathione S-transferases (GSTs) in protecting cells against toxins, xenobiotics, or their metabolites [4]. Te MDR1 gene encodes a member of the ABC transporter subfamily B, a transmembrane P- glycoprotein (P-gp) of 170 kDa, which functions as an adeno- sine triphosphate-dependent efux transporter pump [5]. P- gp is highly expressed on the apical surfaces of superfcial columnar epithelial cells of the colon and distal small bowel. High levels are also found in small biliary ductules and small pancreatic ductules [6]. Te high constitutive levels of P-gp expression in the gut suggest a role as a protective barrier against the absorption of endogenous or exogenous toxins and possibly a putative role in modulation of host- bacterial interactions [7, 8]. Among the polymorphisms identifed in MDR1 gene, the most widely investigated in IBD association studies as well as in other diseases are Hindawi Publishing Corporation Mediators of Inflammation Volume 2015, Article ID 248060, 8 pages http://dx.doi.org/10.1155/2015/248060