| Summary: | 碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 97 === Background: H. pylori - induced inflammation is central to the pathogenesis of all H. pylori - associated diseases. The type IV secretion system of H. pylori delivers peptidoglycan into the host cells, which can then be sensed by the intracellular receptor NOD1 (nucleotide-biding oligomerization domain-containing protein 1), leading to NF-κB activation and consequent IL-8 (interleukin 8) production. It had been reported NOD1 G796A and IL-8 -251 A/T polymorphism were important in H. pylori - induced peptic ulcer. However, the results were inconclusive. The aim of this study was to evaluate the role of NOD1 G796A and IL-8 -251 A/T genetic polymorphism in the development of H. pylori -induced peptic ulcer diseases in Taiwan.
Materials and Methods: 146 patients with endoscope and CLO test (Campylobacter like organism test) were enrolled in the study. NOD1 G796A and IL-8 -251 A/T polymorphism were typed by PCR restriction fragment length polymorphism, TaqMan® SNP genotyping assays (real-time PCR) and multilocus sequence typing.
Results: Old age was significantly associated with gastric ulcer in our study population. Duodenal ulcer was associated with H. pylori infection and gender. The prevalence of duodenal ulcer was higher in male. The H. pylori infection rate was similar in male and in female. Male NOD1 796A carriers and male IL-8 -251A carriers significantly had higher risk of H. pylori-induced duodenal ulcer. Since the genotype distribution was similar in H. pylori-infected male and female, polymorphism and gender may be independent factors of H. pylori-induced duodenal ulcer. There was no association between the polymorphism and H. pylori-induced gastric ulcer.
Conclusion: NOD1 796A carriers and IL-8 -251A carriers significantly had higher risk of H. pylori-induced duodenal ulcer in male. However, it still needs further studies to clarify whether genotype or gender-related- factor plays a major role of H. pylori-induced duodenal ulcer in advance.
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