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Background <p>The host’s immune response to <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection is largely determined by its cytokine profile. Genetic variations within crucial immunomodulatory genes, including those for interleukin-10 (IL-10) and interleukin-12 (IL-12), are thought to influence an individual’s vulnerability to the infection and its clinical consequences by modifying cytokine production. Nonetheless, research data derived from diverse human populations continue to show inconsistent results.</p> Aim <p>This case-control analysis sought to examine a potential link between symptomatic <i>H. pylori</i> infection susceptibility in an Iranian population and specific genetic variants in the IL-10 (-1082G &gt; A, -819&#xa0;C &gt; T) and IL-12 (+ 1188&#xa0;A &gt; C) genes.</p> Methods <p>In this investigation, 68 individuals with confirmed symptomatic <i>H. pylori</i> infection diagnosed by a positive rapid urease test and elevated anti-<i>H. pylori</i> IgG levels exceeding 90 ng/ml via ELISA were enrolled alongside 68 healthy controls. The control group was carefully matched to the patient group based on age, sex, and ethnic background. Genotyping for the IL-10 (-1082G &gt; A, -819&#xa0;C &gt; T) and IL-12 (+ 1188&#xa0;A &gt; C) polymorphisms was conducted using the Amplification Refractory Mutation System-PCR (ARMS-PCR) method. To evaluate associations, the distribution of genotypes and alleles between the groups was contrasted using logistic regression, applying additive, dominant, and recessive inheritance models. The strength of any association was expressed as odds ratios (ORs) accompanied by 95% confidence intervals (CIs).</p> Results <p>The analysis revealed no statistically significant correlations linking the investigated IL-10 and IL-12 gene variants to an increased predisposition for <i>H. pylori</i> infection. A notable methodological observation was the deviation from Hardy-Weinberg equilibrium (HWE) across all studied polymorphisms in the control group. Regarding the IL-10 -1082G &gt; A locus, the AA genotype was associated with a marginally elevated risk estimate; however, this finding was not statistically significant (OR = 3.45, 95% CI: 0.29–41.36; <i>p</i> = 0.327). Likewise, for the IL-12 + 1188&#xa0;A &gt; C polymorphism, the CC genotype, while more prevalent in the patient cohort, also demonstrated no significant association with infection risk (OR = 1.43, 95% CI: 0.42–4.87; <i>p</i> = 0.567).</p> Conclusion <p>This investigation did not establish a significant link between the specific IL-10 and IL-12 gene variants analyzed and susceptibility to symptomatic <i>H. pylori</i> infection in the studied population. Although minor genetic associations were noted, they lacked statistical significance. Future research with larger sample sizes is required to validate these results and to investigate additional genetic determinants that may affect infection risk.</p>

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Association of IL-10 promoter and IL-12 gene polymorphisms with the risk of symptomatic Helicobacter pylori infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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  • Pezhman Karami,
  • Sama Mokari,
  • Mohammad Yousef Alikhani,
  • Sima Kazemi,
  • Mina Mirzaei,
  • Alireza Soltanian,
  • Mohammad Ahmadyousefi,
  • Fereshteh Dehdar,
  • Alireza Rastgoo Haghi,
  • Ebrahim Azizi

摘要

Background

The host’s immune response to Helicobacter pylori (H. pylori) infection is largely determined by its cytokine profile. Genetic variations within crucial immunomodulatory genes, including those for interleukin-10 (IL-10) and interleukin-12 (IL-12), are thought to influence an individual’s vulnerability to the infection and its clinical consequences by modifying cytokine production. Nonetheless, research data derived from diverse human populations continue to show inconsistent results.

Aim

This case-control analysis sought to examine a potential link between symptomatic H. pylori infection susceptibility in an Iranian population and specific genetic variants in the IL-10 (-1082G > A, -819 C > T) and IL-12 (+ 1188 A > C) genes.

Methods

In this investigation, 68 individuals with confirmed symptomatic H. pylori infection diagnosed by a positive rapid urease test and elevated anti-H. pylori IgG levels exceeding 90 ng/ml via ELISA were enrolled alongside 68 healthy controls. The control group was carefully matched to the patient group based on age, sex, and ethnic background. Genotyping for the IL-10 (-1082G > A, -819 C > T) and IL-12 (+ 1188 A > C) polymorphisms was conducted using the Amplification Refractory Mutation System-PCR (ARMS-PCR) method. To evaluate associations, the distribution of genotypes and alleles between the groups was contrasted using logistic regression, applying additive, dominant, and recessive inheritance models. The strength of any association was expressed as odds ratios (ORs) accompanied by 95% confidence intervals (CIs).

Results

The analysis revealed no statistically significant correlations linking the investigated IL-10 and IL-12 gene variants to an increased predisposition for H. pylori infection. A notable methodological observation was the deviation from Hardy-Weinberg equilibrium (HWE) across all studied polymorphisms in the control group. Regarding the IL-10 -1082G > A locus, the AA genotype was associated with a marginally elevated risk estimate; however, this finding was not statistically significant (OR = 3.45, 95% CI: 0.29–41.36; p = 0.327). Likewise, for the IL-12 + 1188 A > C polymorphism, the CC genotype, while more prevalent in the patient cohort, also demonstrated no significant association with infection risk (OR = 1.43, 95% CI: 0.42–4.87; p = 0.567).

Conclusion

This investigation did not establish a significant link between the specific IL-10 and IL-12 gene variants analyzed and susceptibility to symptomatic H. pylori infection in the studied population. Although minor genetic associations were noted, they lacked statistical significance. Future research with larger sample sizes is required to validate these results and to investigate additional genetic determinants that may affect infection risk.