Abstract
BackgroundInflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract. It is fundamentally related to a dysregulated immune response in the intestinal mucosa against microbiota in genetically predisposed individuals. Among the genetic and immunological factors that are suggested to have role in etiology and pathogenesis of IBD are human leukocyte antigen (HLA)-G molecules. Therefore, soluble HLA-G (sHLA-G) serum level and genetic association with HLA-G 14-bp insertion (Ins)/deletion (Del) polymorphism was analyzed in 100 IBD patients; 50 ulcerative colitis (UC) and 50 Crohn’s disease (CD), and 100 controls.ResultssHLA-G level was significantly elevated in IBD patients compared to controls (174.7 ± 27.1 vs. 126.8 ± 15.1; corrected probability [pc] < 0.001). The level was also elevated in UC patients compared to CD patients but the difference was not significant (180.5 ± 27.1 vs. 168.9 ± 26.3; p = 0.059). Receiver operating characteristic analysis confirmed the significance of sHLA-G in total IBD, UC, and CD patients (area under curve = 0.944, 0.961, and 0.927, respectively). The genetic association was analyzed under five genetic models (allele, recessive, dominant, overdominant, and codominant). At the allele level, Del allele frequency was significantly increased in total IBD patients (Odds ratio [OR] = 1.93; 95% confidence interval [CI] = 1.27–2.94; pc = 0.018) and CD patients (OR = 2.08; 95% CI = 1.23–3.54; pc = 0.042) compared to controls. Among UC patients, a similar increased frequency was observed, but the pc value was not significance (OR = 1.79; 95% CI = 1.07–3.00; p = 0.031). At the genotypic level, Del/Del genotype was associated with a significantly increased IBD-risk in total patients under codominant model (OR = 4.06; 95% CI = 1.56–10.56; pc = 0.024). sHLA-G level was not influenced by the Ins/Del polymorphism.ConclusionsThis study demonstrated a significant increase in serum level of sHLA-G in UC and CD patients. Further, HLA-G 14-bp Ins/Del polymorphism may be associated with susceptibility to IBD, particularly CD.
Highlights
Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract
Among the genetic and immunological factors that are proposed to have a role in etiology and pathogenesis of IBD are human leukocyte antigen (HLA)-G molecules, which are encoded by the non-classical major histocompatibility (MHC) class I genes that are mapped to the short arm of chromosome 6 (6p21.3) [5,6,7]
With regard to disease extension, ulcerative colitis (UC) patients were classified as ulcerative proctitis (40%), left-sided colitis (30%), and extensive colitis (30%), while most of Crohn’s disease (CD) patients were classified under ileocecal colitis (86%)
Summary
Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract. The inflammation in UC is restricted to the colon and rectum, while in CD, it involves any part of the gastrointestinal tract in a noncontinuous fashion [2] Their clinical presentations are similar, but diarrhea and bleeding are most likely presented in UC, whereas watery diarrhea and vague symptoms are encountered in CD [3]. Etiology of both phenotypes is incompletely understood, but complex interactions between genetic, environmental, immunological, and gut microbiomial factors are suggested to be involved. Their interactions orchestrate a cascade of inflammatory responses in the intestinal mucosa [4]. Among the genetic and immunological factors that are proposed to have a role in etiology and pathogenesis of IBD are human leukocyte antigen (HLA)-G molecules, which are encoded by the non-classical major histocompatibility (MHC) class I genes that are mapped to the short arm of chromosome 6 (6p21.3) [5,6,7]
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