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An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
A pro-inflammatory genotype predisposes to Barrett's esophagus
L M G Moons1, J G Kusters, J H M van Delft
1Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center Rotterdam, Postbus 2040, 3000 CA Rotterdam, the Netherlands.
Carcinogenesis
|January 15, 2008
Summary
Genetic variations in cytokine genes, specifically interleukin-12B (IL-12B) and interleukin-10 (IL-10), are linked to Barrett's esophagus (BE) development. A pro-inflammatory genetic profile, especially with a hiatal hernia, increases BE risk.
Area of Science:
- Gastroenterology
- Genetics
- Immunology
Background:
- Mucosal inflammation severity is linked to Barrett's esophagus (BE) development in animal models.
- A strong pro-inflammatory host response is postulated to predispose individuals to BE.
Purpose of the Study:
- To investigate the association between cytokine gene polymorphisms and the development of BE.
- To determine the specific cytokine genes influencing BE susceptibility.
Main Methods:
- Multiplex SNaPshot method used to genotype polymorphisms in IL-12B, IL-10, IL-8, IL-6, and IL-2 genes.
- Study included 255 BE patients and 247 reflux esophagitis (RE) patients.
Main Results:
- The IL-12B C-allele (associated with increased IL-12p70) was more frequent in BE patients (OR 1.8).
- BE risk increased with IL-12B C-allele and hiatal hernia (OR 2.9).
- IL-10 GG genotype (higher IL-10) showed decreased BE risk with IL-12B C-allele, suggesting IL-10-dependent down-regulation.
Conclusions:
- A genetic profile favoring a pro-inflammatory response (IL-12p70, IL-10) is associated with BE.
- Coincidence of this genetic profile with hiatal hernia amplifies BE risk.
- Gastroesophageal reflux in individuals with a pro-inflammatory genetic background drives BE development.
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