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Updated: Jun 8, 2026

Fluorescence-mediated Tomography for the Detection and Quantification of Macrophage-related Murine Intestinal Inflammation
Published on: December 15, 2017
Functional promoter polymorphisms of macrophage migration inhibitory factor in peptic ulcer diseases
Hisakazu Shiroeda1, Tomomitsu Tahara, Tomoyuki Shibata
1Department of Gastroenterology, Kanazawa Medical University, Uchinada-machi, Ishikawa 920-0293, Japan.
Abstract:
Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator, which plays a pivotal role in inflammatory and immune diseases. We attempted to clarify the association of functional polymorphisms of MIF gene promoter with the development of gastro-duodenal ulcer. The study was performed in 471 stocked DNAs obtained from the subjects, including 93 healthy volunteers, with no evidence of gastric malignancy. We employed the PCR-SSCP method to detect gene polymorphisms. In all 471 DNAs, 92 and 43 were obtained from gastric and duodenal ulcer patients, respectively. By an unadjusted analysis, infection with Helicobacter pylori (H. pylori), male gender and non-steroidal anti-inflammatory drug (NSAID/aspirin) use were significantly associated with a risk for developing a gastric ulcer, whereas MIF promoter polymorphisms were not. On the other hand, infection with H. pylori, male gender and 7-CATT repeat at position -794 were significantly associated with the development of a duodenal ulcer, whereas NSAID/ aspirin use was not. By the analysis after adjustment for age, gender, NSAID/aspirin use and H. pylori infection status, 7/7-CATT homozygote had a significantly increased risk for the development of duodenal ulcers (OR, 6.31; 95% CI, 1.50-26.6; p=0.012). No factors were significantly associated with the development of peptic ulcers in NSAID/aspirin users. Our results suggested that tetranucleotide repeat polymorphism of MIF gene promoter might be associated with the development of duodenal ulcers.
Insights
Macrophage migration inhibitory factor (MIF) gene promoter polymorphisms are linked to duodenal ulcers. Specifically, the 7/7-CATT homozygote genotype increases the risk of developing duodenal ulcers, independent of H. pylori infection.
Area of Science:
- Genetics
- Immunology
- Gastroenterology
Background:
- Macrophage migration inhibitory factor (MIF) is a critical pro-inflammatory mediator involved in immune and inflammatory diseases.
- Gastro-duodenal ulcers are common conditions influenced by genetic and environmental factors.
Purpose of the Study:
- To investigate the association between functional polymorphisms in the MIF gene promoter and the development of gastro-duodenal ulcers.
- To identify genetic risk factors for duodenal ulcer development.
Main Methods:
- A case-control study involving 471 DNA samples from healthy volunteers and patients with gastric or duodenal ulcers.
- Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) was used to detect MIF gene promoter polymorphisms.
- Statistical analysis, including unadjusted and adjusted models, was performed to assess associations with ulcer development.
Main Results:
- Helicobacter pylori (H. pylori) infection, male gender, and NSAID/aspirin use were associated with gastric ulcer risk, but not MIF polymorphisms.
- H. pylori infection, male gender, and the 7-CATT repeat polymorphism at position -794 of the MIF gene promoter were associated with duodenal ulcer development.
- The 7/7-CATT homozygote genotype showed a significantly increased risk for duodenal ulcers after adjusting for confounding factors (OR, 6.31; 95% CI, 1.50-26.6; p=0.012).
Conclusions:
- Tetranucleotide repeat polymorphism in the MIF gene promoter is associated with an increased risk of developing duodenal ulcers.
- The 7/7-CATT homozygote genotype represents a potential genetic susceptibility factor for duodenal ulcers.
- Further research is warranted to elucidate the precise mechanisms linking MIF gene polymorphisms to duodenal ulcer pathogenesis.
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