<p>Allergic rhinitis (AR), a highly prevalent inflammatory disorder of the upper respiratory tract, demonstrates strong genetic determinants. <i>TLR6</i> and <i>NFKB1</i> variants were genotyped to assess the associations with AR susceptibility. Blood samples from 992 AR patients and 992 matched healthy controls were collected for SNPs genotyping via Agena MassARRAY system. Associations were evaluated using logistic regression to calculate odds ratios (OR) with 95% confidence intervals (CI). Significant findings were evaluated by false positive reporting probability (FPRP) analysis (threshold = 0.2; prior probability = 0.1). Relationships between polymorphisms and clinical features were analyzed using analysis of Variance (ANOVA). <i>NFKB1</i> rs230504 (<i>p</i> = 0.016, OR = 0.72) and rs4648052 (<i>p</i> = 0.011, OR = 0.85) demonstrated protective effects against AR risk. Stratified analyses revealed the risk-reducing-association of <i>NFKB1</i> rs4648052 with AR occurrence in individuals ≤ 43&#xa0;years, men, and those with BMI &gt; 24&#xa0;kg/m<sup>2</sup>. <i>NFKB1</i> rs230504 conferred protection for AR susceptibility in men and participants with BMI ≤ 24&#xa0;kg/m<sup>2</sup>. Moreover, <i>TLR6</i> rs3796508 contributed to the increased AR risk in women. The protective effects of <i>NFKB1</i> rs230504 and rs4648052 against AR susceptibility remained noteworthy. The relation of <i>TLR6</i> rs3796508 and rs5743808 genotypes to high density lipoprotein (HDL) levels in controls. <i>NFKB1</i> rs230504 genotypes correlated with HDL and fasting blood glucose levels in controls. This study identified <i>NFKB1</i> rs230504 and rs4648052 as protective variants against AR development in China’s Han population, advancing understanding of genetic mechanisms in AR pathogenesis.</p>

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NFKB1 genetic variation and allergic rhinitis susceptibility: a study in the Chinese Han population

  • Haiying Wang,
  • Chunyan Wang,
  • Huimin Yang,
  • Lizhen Liu,
  • Jinqi Hao,
  • Yonglin Liu

摘要

Allergic rhinitis (AR), a highly prevalent inflammatory disorder of the upper respiratory tract, demonstrates strong genetic determinants. TLR6 and NFKB1 variants were genotyped to assess the associations with AR susceptibility. Blood samples from 992 AR patients and 992 matched healthy controls were collected for SNPs genotyping via Agena MassARRAY system. Associations were evaluated using logistic regression to calculate odds ratios (OR) with 95% confidence intervals (CI). Significant findings were evaluated by false positive reporting probability (FPRP) analysis (threshold = 0.2; prior probability = 0.1). Relationships between polymorphisms and clinical features were analyzed using analysis of Variance (ANOVA). NFKB1 rs230504 (p = 0.016, OR = 0.72) and rs4648052 (p = 0.011, OR = 0.85) demonstrated protective effects against AR risk. Stratified analyses revealed the risk-reducing-association of NFKB1 rs4648052 with AR occurrence in individuals ≤ 43 years, men, and those with BMI > 24 kg/m2. NFKB1 rs230504 conferred protection for AR susceptibility in men and participants with BMI ≤ 24 kg/m2. Moreover, TLR6 rs3796508 contributed to the increased AR risk in women. The protective effects of NFKB1 rs230504 and rs4648052 against AR susceptibility remained noteworthy. The relation of TLR6 rs3796508 and rs5743808 genotypes to high density lipoprotein (HDL) levels in controls. NFKB1 rs230504 genotypes correlated with HDL and fasting blood glucose levels in controls. This study identified NFKB1 rs230504 and rs4648052 as protective variants against AR development in China’s Han population, advancing understanding of genetic mechanisms in AR pathogenesis.