Przybyłowska Karolina, Mrowicki Jerzy, Sygut Andrzej, Narbutt Piotr, Dziki Łukasz, Dziki Adam, Majsterek Ireneusz
Department of Chemistry and Biochemistry, Medical University in Łódź.
Pol Przegl Chir. 2011 Feb;83(2):76-80. doi: 10.2478/v10035-011-0012-x.
Inflammatory bowel disease (IBD) represents a heterogeneous group of chronic disorders characterized by inflammation of gastrointestinal tract, typically with a relapsing and remitting clinical course of unknown etiology. Presumably, IBD develops with response exogenous environmental factors only in persons with genetic predisposition. This predisposition was suggested to be associated with polymorphism and mutations in genes encoding proinflammatory immune system proteins. Enhanced production of macrophage migration inhibitory factor (MIF) was found in patients with inflammatory bowel disease (IBD) and mice with experimental colitis. These results suggest that MIF plays a critical role in etiology of the colitis.The aim of the study was determine whether the MIF -173 G/C gene polymorphism is associated with the susceptibility to inflammatory bowel disease (IBD).
A total of 99 IBD patients, including 58 patients with ulcerative colitis (UC) and 41 with Crohn's disease (CD) and 436 healthy controls recruited from the Polish population, were genotyped for MIF polymorphisms. Genotyping of MIF gene polymorphism was performed by a RFLP-PCR.
We found an increased risk of UC for the C allele of the MIF-173 G/C polymorphism. The distribution of the genotypes was not significantly different in the CD group compared with the controls.
We demonstrated that the C allele is associated with an increased risk for development of UC. This suggests that the G/C polymorphism in the MIF gene promoter may be a potential risk factor for UC in Polish population.
炎症性肠病(IBD)是一组异质性慢性疾病,其特征为胃肠道炎症,临床病程通常呈复发和缓解,病因不明。据推测,IBD仅在具有遗传易感性的个体中因外源性环境因素而发病。这种易感性被认为与编码促炎免疫系统蛋白的基因中的多态性和突变有关。在炎症性肠病(IBD)患者和实验性结肠炎小鼠中发现巨噬细胞移动抑制因子(MIF)的产生增加。这些结果表明MIF在结肠炎的病因中起关键作用。本研究的目的是确定MIF -173 G/C基因多态性是否与炎症性肠病(IBD)的易感性相关。
从波兰人群中招募了99例IBD患者,包括58例溃疡性结肠炎(UC)患者和41例克罗恩病(CD)患者以及436名健康对照,对其进行MIF多态性基因分型。通过RFLP-PCR进行MIF基因多态性的基因分型。
我们发现MIF-173 G/C多态性的C等位基因使UC发病风险增加。与对照组相比,CD组的基因型分布无显著差异。
我们证明C等位基因与UC发病风险增加相关。这表明MIF基因启动子中的G/C多态性可能是波兰人群中UC的潜在危险因素。