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Host Single Nucleotide Polymorphisms of MMP-9 −1562/TIMP-1 372 Have Gender Differences in the Risk of Gastric Intestinal Metaplasia After Helicobacter pylori Infection

Background:  Helicobacter pylori infection causes chronic gastric inflammation and intestinal metaplasia (IM), related with deregulation of Wnt pathway and over‐expressions of COX‐2, matrix metalloproteinase (MMP), and tissue inhibitors of matrix metalloproteinase (TIMP). We thus test the host genom...

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Published in:Helicobacter (Cambridge, Mass.) Mass.), 2009-12, Vol.14 (6), p.580-587
Main Authors: Hung, Kuei-Hsiang, Hung, Hunt-Wen, Yang, Hsiao-Bai, Lu, Cheng-Chan, Wu, Jiunn-Jong, Sheu, Bor-Shyang
Format: Article
Language:English
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Summary:Background:  Helicobacter pylori infection causes chronic gastric inflammation and intestinal metaplasia (IM), related with deregulation of Wnt pathway and over‐expressions of COX‐2, matrix metalloproteinase (MMP), and tissue inhibitors of matrix metalloproteinase (TIMP). We thus test the host genomic predispositions related to the risk of IM after H. pylori infection. Methods:  We enrolled 296 H. pylori‐infected patients to provide gastric biopsies for histology and genomic DNA for genotypes of single nucleotide polymorphisms (SNPs), including APC, COX‐2, IL‐1B, IL‐1RN, IL‐10, MMP‐2, MMP‐9, TIMP‐1, and TIMP‐2 determined by sequence specific oligonucleotide probe, sequence specific primers, restriction fragment length polymorphism, or real‐time polymerase chain reaction. Results:  There was no association between the presence of IM and SNPs in APC, COX‐2, IL‐1B, IL‐1RN, IL‐10, MMP‐2, and TIMP‐2. The risk of IM was increased up to 2.29‐folds in males with TIMP‐1 372 C, and 3.03‐fold in females with T carrier (p 
ISSN:1083-4389
1523-5378
DOI:10.1111/j.1523-5378.2009.00717.x