Contribution of the -173 G/C Polymorphism of Macrophage Migration Inhibitory Factor Gene to the Risk of Inflammatory Bowel Diseases

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Contribution of the -173 G/C Polymorphism of Macrophage Migration Inhibitory Factor Gene to the Risk of Inflammatory Bowel Diseases

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).

Material and methods. 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.

Results. 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.

Conclusions. 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.

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Polish Journal of Surgery

The Journal of Foundation of the Polish Journal of Surgery

Journal Information

CiteScore 2016: 0.29

SCImago Journal Rank (SJR) 2016: 0.166
Source Normalized Impact per Paper (SNIP) 2016: 0.207


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