Influence of IL-1 gene cluster polymorphisms on the development of H. pylori associated gastric ulcer
Chronic H. pylori infection is the main cause of ulcer disease which depicts a major burden of our healthy care systems. The individual host immune response plays a pivotal role in the outcome of the infection but genetic susceptibility to develop gastric ulcer is unknown. IL-1β and its natural rece...
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Veröffentlicht in: | Immunology Letters 2005-09, Vol.100 (2), p.107-112 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Chronic
H. pylori infection is the main cause of ulcer disease which depicts a major burden of our healthy care systems. The individual host immune response plays a pivotal role in the outcome of the infection but genetic susceptibility to develop gastric ulcer is unknown. IL-1β and its natural receptor antagonist IL-1ra are involved in the inflammatory response to
H. pylori infection. Thus, we investigated the influence of functional genetic variants in the IL-1 gene cluster on the development of gastric ulcer disease.
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H. pylori infected patients were genotyped for IL-1B −31 and +3954 by TaqMan technology. Alleles of IL-1RN 86VNTR were determined by gel electrophoresis after amplification. Three hundred and sixty healthy blood donors were included as healthy controls.
Carriage of the IL-1B −31 C allele conferred a increased but not significant risk for
H. pylori infection (OR: 1.3, Wald 95% CI: 0.8
<
OR
<
2.1). Patients carrying short allele 2 of IL-1RN had a 1.6-fold significantly increased risk for the development of gastric ulcer (Pearson's
=
4.0,
p
=
0.044, OR: 1.6, Wald 95% CI: 1.0
<
OR
<
2.4).
Our results underline the crucial role of the host immune response to
H. pylori infection and confirm the importance of polymorphisms in the IL-1 cluster as a factor to give rise to different clinical outcomes. Further studies are needed to fully understand the pathophysiological effect of polymorphisms in the IL-1 cluster in
H. pylori associated ulcer disease and susceptibility to infection itself. |
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ISSN: | 0165-2478 1879-0542 1365-2567 |
DOI: | 10.1016/j.imlet.2005.04.001 |