
@Article{,
AUTHOR = {Zsoﬁa Gyulai, Gergely Klausz, Andrea Tiszai, Zsuzsanna Lénárt, Izabella Tóth Kása, János Lonovics, Yvette Mándi},
TITLE = {Genetic polymorphism of interleukin-8 (IL-8) is associated with <i>Helicobacter pylori</i>-induced duodenal ulcer},
JOURNAL = {European Cytokine Network},
VOLUME = {15},
YEAR = {2004},
NUMBER = {4},
PAGES = {353--358},
URL = {http://www.techscience.com/ECN/v15n4/66367},
ISSN = {1952-4005},
ABSTRACT = {Background and aims. Helicobacter pylori infection almost invariably causes chronic gastritis, but
only a proportion of the infected subjects develop peptic ulcers. The local inﬂammation associated with <i>H. pylori</i>
infection is characterized by an increased production of the proinﬂammatory cytokines IL-1–B, IL-6, IL-8 and
TNF-α. Since such cytokine production is often determined by the genetic polymorphism of regions regulating
cytokine gene expression, we investigated the relationship between TNF-α and IL-8 polymorphisms and the
development of duodenal ulcer disease. We also sought a correlation between the promoter polymorphism of the
lipopolysaccharide (LPS) receptor CD14 and the formation of peptic ulcer, because CD14 plays a crucial role in
the initiation of the cytokine cascade. Methods. Genomic DNA extracted from the peripheral blood of 69 patients
with <i>H. pylori</i>-positive duodenal ulcer disease and 47 <i>H. pylori</i>-positive healthy controls was analyzed for TNF-α
-308 promoter polymorphism by RFLP, and for IL-8 -251 polymorphism by ARMS. Genetic polymorphism within
the promoter of the CD14 gene was identiﬁed using the LightCycler instrument via melting point analysis. Results:
No signiﬁcant correlation could be revealed between the TNF-α and CD14 promoter polymorphisms and the
clinical outcome of <i>H. pylori</i> infection. The IL-8 A/T heterozygote mutant variant was detected with a signiﬁcantly
higher frequency (65.22%) among the ulcer patients than among the healthy, <i>H. pylori</i>-positive blood donors
(36.17%), while the frequency of the normal allelic genotype (TT) was signiﬁcantly higher in the control group
(44.6% vs 15.9%). Conclusion. Analysis of the genetic predisposition to enhanced cytokine production revealed a
signiﬁcant association only for the IL-8 polymorphism. This observation draws attention to the possible
importance of IL-8 polymorphism as a genetic predisposing factor in the pathomechanism of <i>H. pylori</i>-induced
duodenal ulcer disease, and to the relative protection from duodenal ulcer disease that is associated with the TT
genotype.},
DOI = {}
}



