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Low Expression Myeloperoxidase Genotype Negatively Associated with Helicobacter pylori Infection
Our previous study revealed that a polymorphism of the interleukin (IL) 1B gene, encoding the pro‐inflammatory cytokine IL‐lβ, influenced the prevalence of persistent Helicobacter pylori (HP) infection. In this paper, a polymorphism of another inflammation‐related enzyme, myeloperoxidase (MPO), was...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2001
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5926737/ https://www.ncbi.nlm.nih.gov/pubmed/11376556 http://dx.doi.org/10.1111/j.1349-7006.2001.tb01120.x |
Sumario: | Our previous study revealed that a polymorphism of the interleukin (IL) 1B gene, encoding the pro‐inflammatory cytokine IL‐lβ, influenced the prevalence of persistent Helicobacter pylori (HP) infection. In this paper, a polymorphism of another inflammation‐related enzyme, myeloperoxidase (MPO), was examined with respect to association with the HP infection. The polymorphism is due to a G‐to‐A transition at ‐463 in the promoter region of MPO. The G allele is the wild type with normal expression, while the A allele is a low expression allele. The subjects were 241 non‐cancer outpatients (118 males and 123 females) aged 39 to 69 who participated in an HP eradication program at Aichi Cancer Center Hospital. High‐molecular weight Campylobacter‐Associated‐Protein (HM‐CAP) ELISA (Enteric Products Ins., Westbury, NY) was used for the identification of HP‐infected participants. The frequency was 79.7% (192/241) for the GG genotype, 19.5% (47/241) for the GA genotype, and 0.8% (2/241) for the AA genotype. The sex‐age‐adjusted odds ratio (OR) relative to GG was 0.69 (95% confidence interval (CI), 0.35–1.35) for individuals with the A allele, but among male participants the OR was 0.31 (0.11–0.84). Subgroup analysis revealed significantly reduced ORs with the GA/AA genotypes for current smokers (0.19, 0.04–0.96), and for those who were occasional/no milk drinkers (0.25, 0.09–0.72). These findings are consistent with the results for IL‐1B in our earlier study, suggesting that inflammatory responses in the gastric mucosa may influence persistent HP infection, and that smoking and milk intake may be effect ‐modifiers. |
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