The study has a limitation of just providing 181 isolates for the

The study has a limitation of just providing 181 isolates for the analysis of the dupA status of H. pylori, which disclose a rather low 20% dupA-positive prevalence rate. Accordingly, the study S3I-201 in vitro became limited to only 103 patients to provide both analyses

on the infected isolate’s dupA status and the host’s SNPs (Figure 2). It thus cannot provide an adequate statistical power to determine the exact impact of MMP-3 SNPs under dupA-negative specific conditions. Conclusions In conclusion, this study provides evidence that host promoter polymorphisms of MMP-3 contribute to increased individual susceptibility to duodenal ulcers in females after H. pylori infection in Taiwan. The MMP-3 promoter genotypes may serve to screen out patients at risk and target for H. pylori eradication in order to stop the ulceration process among H. pylori-infected patients without ulcers yet. Acknowledgements This study was supported by grants from the National Science Council, Taiwan (95-2314-B-006-029-MY3 and 98-2628-B-006-013-MY3), NHRI-EX99-9908BI from the National Health Research Institute, and DOH99-TD-C-111-003 from Department of Health, Taiwan. The authors also thank Miss Hunt-Wen Wu for her assistance. References 1. Labigne A, de Reuse H: Determinants of Helicobacter pylori pathogenicity. Infect Agents Dis 1996,5(4):191–202.PubMed 2. Maeda S, Mentis AF: Pathogenesis MG-132 ic50 of Helicobacter pylori infection. Helicobacter

2007,12(Suppl 1):10–14.PubMedCrossRef 3. Prinz C, Schwendy S, Voland P: H. pylori and gastric cancer: shifting the global burden. World J Gastroenterol 2006,12(34):5458–5464.PubMed 4. Sheu BS, Odenbreit S, Hung KH, Liu CP, Sheu SM, Yang HB, Wu JJ: Interaction between tuclazepam host gastric Sialyl-Lewis X and H. pylori SabA enhances H. pylori density in patients lacking gastric Lewis B antigen. Am J Gastroenterol 2006,101(1):36–44.PubMedCrossRef 5. Lai CH, Kuo CH, Chen YC, Chao FY, Poon SK, Chang

CS, Wang WC: High prevalence of cagA – and babA2 -positive Helicobacter pylori clinical isolates in Taiwan. J Clin Microbiol 2002,40(10):3860–3862.PubMedCrossRef 6. Lu H, Hsu PI, Graham DY, Yamaoka Y: Duodenal ulcer promoting gene of Helicobacter pylori . Gastroenterology 2005,128(4):833–848.PubMedCrossRef 7. Schmidt HM, Andres S, Nilsson C, Kovach Z, Kaakoush NO, Engstrand L, Goh KL, Fock KM, Forman D, Mitchell H: The cag PAI is intact and functional but HP0521 varies significantly in Helicobacter pylori isolates from Malaysia and Singapore. Eur J Clin Microbiol Infect Dis 2010,29(4):439–451.PubMedCrossRef 8. Nguyen LT, Uchida T, Tsukamoto Y, Kuroda A, Okimoto T, Kodama M, Murakami K, Fujioka T, Moriyama M: Helicobacter pylori dupA gene is not associated with clinical outcomes in the Japanese population. Clin Microbiol Infect 2010,16(8):1264–1269.PubMedCrossRef 9. Hussein NR: The association of dupA and Helicobacter pylori -related gastroduodenal diseases. Eur J Clin Microbiol Infect Dis 2010,29(7):817–821.PubMedCrossRef 10.

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