Inflammatory 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. sHLA-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. This 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.

中文翻译：

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可溶性 HLA-G 和 HLA-G 14-bp 插入/缺失多态性在炎症性肠病中的易感性作用

炎症性肠病 (IBD) 是一组胃肠道慢性炎症性疾病。它从根本上与肠道粘膜中针对遗传易感个体的微生物群的失调免疫反应有关。人类白细胞抗原 (HLA)-G 分子被认为在 IBD 的病因和发病机制中起作用的遗传和免疫学因素之一。因此，在 100 名 IBD 患者中分析了可溶性 HLA-G (sHLA-G) 血清水平和与 HLA-G 14-bp 插入 (Ins)/缺失 (Del) 多态性的遗传关联；50 名溃疡性结肠炎 (UC) 和 50 名克罗恩病 (CD)，以及 100 名对照。与对照组相比，IBD 患者的 sHLA-G 水平显着升高（174.7 ± 27.1 与 126.8 ± 15.1；校正概率 [pc] < 0.001）。与 CD 患者相比，UC 患者的水平也升高，但差异不显着（180.5 ± 27.1 对 168.9 ± 26.3；p = 0.059）。接受者操作特征分析证实了 sHLA-G 在总 IBD、UC 和 CD 患者中的显着性（曲线下面积分别为 0.944、0.961 和 0.927）。在五种遗传模型（等位基因、隐性、显性、过度显性和共显性）下分析了遗传关联。在等位基因水平上，总 IBD 患者（比值比 [OR] = 1.93；95% 置信区间 [CI] = 1.27–2.94；pc = 0.018）和 CD 患者（OR = 2.08；95%）的 Del 等位基因频率显着增加与对照相比，CI = 1.23–3.54；pc = 0.042)。在 UC 患者中，观察到类似的增加频率，但 pc 值不显着（OR = 1.79；95% CI = 1.07–3.00；p = 0.031）。在基因型水平上，Del/Del 基因型与共显性模型下所有患者的 IBD 风险显着增加相关（OR = 4.06；95% CI = 1.56–10.56；pc = 0.024）。sHLA-G 水平不受 Ins/Del 多态性的影响。该研究表明 UC 和 CD 患者血清 sHLA-G 水平显着增加。此外，HLA-G 14-bp Ins/Del 多态性可能与 IBD 易感性有关，尤其是 CD。