However, even in such large-scale validation, those with duodenal ulcer have a nearly 55% dupA-positive infection [6]. Moreover, prevalence of dupA and relationships between dupA-positive H. pylori and clinical outcomes are different in distinct populations [7–11]. It may indicate that dupA serves a promoting role leading to duodenal ulcer after H. pylori infection. Alternatively, it is necessary to validate host factors that predispose patients to gastroduodenal ulcer,

especially with dupA-negative infection. H. pylori infection stimulates the production of pro-inflammatory cytokines, Erismodegib datasheet such as IL-1, which play important roles in gastric inflammation and physiology. However, IL-1 beta or IL-1RN polymorphisms are not associated with gastric ulcer in the Taiwanese population [12]. Matrix metalloproteinases (MMPs) are a family NSC23766 clinical trial of enzymes that degrade most extracellular matrix and correlate with ulcer formation or repairs [13]. H. pylori infection can up-regulate MMP-3, MMP-7, and MMP-9 in the gastric mucosa and even sera [14–16]. A large-scale German survey has further validated that the single-nucleotide polymorphisms

(SNP) genotype as MMP-7-181 G allele and MMP-9exon 6 A allele increase the risk of gastric ulcer after H. pylori infection [17]. A deletion at MMP-3 promoter -1612, and A to G substitution at MMP-7 promoter -181 may affect transcriptional activity, leading to alterations in gene expression [18, 19]. Moreover, A to G substitution at MMP-9 exon 6 causes the amino acid PND-1186 price change required for binding to its substrate

and affects its binding ability [20]. Although MMP activity is in general counteracted by endogenous tissue inhibitors (TIMPs) [21], there remains no data to check whether TIMP-1 and TIMP-2 SNP genotypes relate to the risk of gastroduodenal ulcer after H. pylori-infection. As such, this study surveyed if the H. pylori dupA genotype and certain SNP genotypes of MMP-3, MMP-7, MMP-9, TIMP-1, and TIMP-2 predispose H. pylori-infected Taiwanese patients to ulcer risks. Methods Patients and study design Five hundred and forty-nine consecutive H. pylori-infected patients documented by upper gastrointestinal endoscopy at National Cheng Kung University Medical Center, Tainan, Ribonucleotide reductase Taiwan were enrolled. All were genetically unrelated ethnic Han Chinese from Tainan City and the surrounding regions. None had been treated with NSAIDs, proton pump inhibitor, or any antibiotics within two weeks prior to panendoscopy on enrollment, or a past history of anti-H. pylori treatment and peptic ulcer. The hospital Ethics Committee approved the study. After obtaining informed consent, 470 patients had provided enough blood samplings for SNPs analysis of MMP-3-1612 6A > 5A, MMP-7-181 A > G, MMP-9exon 6 A > G, TIMP-1372 T > C and TIMP-2-418 G > C by PCR-RFLP.