1887

Abstract

eradication can reverse gastric intestinal metaplasia (IM) in some but not all patients. induces high levels of nuclear -catenin staining in IM tissues, as well as overexpression of cyclooxygenase-2 (COX-2). This study investigated whether the Wnt/-catenin pathway plays a role in IM regression following eradication. Sixty-five -infected patients with IM who had achieved successful eradication provided paired gastric samples before and after eradication to analyse the persistence of IM, and to assess COX-2 and nuclear -catenin expression. The host genotypes of single nucleotide polymorphisms (SNPs) of the , -catenin () and adenomatous polyposis coli () genes were analysed. In addition, expression of -catenin, E-cadherin and phosphorylated and unphosphorylated glycogen synthase kinase 3 (GSK-3) in cell lines challenged with isolates from patients with and without IM persistence was compared by immunoanalysis. After a mean 33.9-month follow-up after eradication, 44 patients (67.7 %) with IM persistence had a higher rate of high-level nuclear -catenin expression in IM tissue than those without IM persistence (=0.008). The patients with IM persistence had a higher rate of AA, GG and AA SNP genotypes at positions 4479, 5268 and 5465, respectively, than the patients without IM persistence (=0.022). The isolates from the patients with IM regression after eradication induced more phospho-GSK-3 in AGS cells than isolates from patients with IM persistence (=0.011). It is likely that interactions with and the patient's Wnt/-catenin genetic predisposition determine the outcome of IM persistence following eradication.

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2009-05-01
2020-07-16
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