OBJECTIVE: Genetic susceptibility appears to play an important role in Helicobacter pylori (HP) infection. The present study was conducted to re-examine the reported association between the myeloperoxidase (MPO) G-463A polymorphism and HP seropositivity in different subjects and to investigate interactions with smoking behavior and the interleukin-1B (IL-1B) C-31T polymorphism. METHODS: The subjects were 468 health checkup examinees in Nagoya, who consented to anonymous genotyping of residual blood samples. Genotyping was conducted by PCR-RFLP for MPO G-463A and PCR-CTPP for IL-1B C-31T. RESULTS: Among the successfully genotyped 437 participants without a cancer history, the HP seropositive rate was 56.2% for -463GG (n = 354), 49.4% for -463GA (n = 77) and 83.3% for -463AA (n = 6). The gender-age-adjusted odds ratio (aOR) for GA/AA relative to GG was 0.86 (95% confidence interval, 0.32-1.34) among males, 0.84 (0.47-1.49) among females, 0.83 (0.22-3.05) among current smokers and 0.87 (0.50-1.51) among never smokers. Analysis by IL-1B C-31T genotype revealed a significantly reduced OR of 0.41 (0.18-0.93) among the participants with IL-1B -31CT. The OR for IL-1B -31TT relative to -31CC/CT was 1.59 (1.00-2.55) among those with MPO -463GG and 3.36 (1.16-9.77) with MPO -463GA/AA. None of the gene-environment or gene-gene interactions proved to be statistically significant. CONCLUSIONS: The association between MPO G-463A and HP seropositivity was not reproduced in this study. The effect of IL-1B -31TT was more prominent among individuals with the low expression MPO -463A allele, but it remains to be confirmed for other datasets.
OBJECTIVE: Genetic susceptibility appears to play an important role in Helicobacter pylori (HP) infection. The present study was conducted to re-examine the reported association between the myeloperoxidase (MPO) G-463A polymorphism and HP seropositivity in different subjects and to investigate interactions with smoking behavior and the interleukin-1B (IL-1B) C-31T polymorphism. METHODS: The subjects were 468 health checkup examinees in Nagoya, who consented to anonymous genotyping of residual blood samples. Genotyping was conducted by PCR-RFLP for MPO G-463A and PCR-CTPP for IL-1BC-31T. RESULTS: Among the successfully genotyped 437 participants without a cancer history, the HP seropositive rate was 56.2% for -463GG (n = 354), 49.4% for -463GA (n = 77) and 83.3% for -463AA (n = 6). The gender-age-adjusted odds ratio (aOR) for GA/AA relative to GG was 0.86 (95% confidence interval, 0.32-1.34) among males, 0.84 (0.47-1.49) among females, 0.83 (0.22-3.05) among current smokers and 0.87 (0.50-1.51) among never smokers. Analysis by IL-1BC-31T genotype revealed a significantly reduced OR of 0.41 (0.18-0.93) among the participants with IL-1B -31CT. The OR for IL-1B -31TT relative to -31CC/CT was 1.59 (1.00-2.55) among those with MPO -463GG and 3.36 (1.16-9.77) with MPO -463GA/AA. None of the gene-environment or gene-gene interactions proved to be statistically significant. CONCLUSIONS: The association between MPO G-463A and HP seropositivity was not reproduced in this study. The effect of IL-1B -31TT was more prominent among individuals with the low expression MPO -463A allele, but it remains to be confirmed for other datasets.