Association of IL-4 gene polymorphism with serum IgE and eosinophil levels in asthma patients

Abstract

Asthma represents a chronic airway inflammatory disease with a Th2-cell polarization as the major design of immune response, and interleukin-4 (IL-4) is pivotal in IgE production and eosinophilia. Polymorphisms in the IL-4 gene can alter an individual's susceptibility to asthma and its associated immunological markers. The purpose of this study was to determine if there was a relationship between the genotypic distribution in 2 IL-4 gene polymorphic sites and the asthma IgE level and the peripheral eosinophil count. A cross-sectional case-control study was carried out at Al-Sadr Medical City, Najaf, Iraq from March to December 2025, that included 98 asthmatic patients who were diagnosed by the Global Initiative for Asthma (GINA) guidelines and 52 healthy controls age- and sex-matched. Demographic and clinical information was obtained with the help of structured questionnaires. Serum total IgE were quantified by ELISA, eosinophils were determined with an automated hematology analyzer and the IL-4 gene polymorphism was investigated using PCR-RFLP. Serum IgE levels (310.6 ± 118.4 IU/mL vs. 142.3 ± 64.7 IU/mL, P < 0.002) and eosinophil counts (468.2 ±152.6 vs.286·9 _.104.s cellsip1L,:P<0T03,) were significantly higher in asthmatics than in control subjects; The IL-4 T allele, and TC and TT genotypes were significantly higher in asthmatic patients than in control individuals. In addition, the T allele and TT+TC genotype were significantly correlated with higher levels of IgE and eosinophilia in asthmatics. In summary, our results demonstrate that the IL-4 gene polymorphism is associated with asthmatic susceptibility and important immunological mechanisms of asthma such as total IgE production and eosinophilic inflammation. These findings reinforce the contribution of genetic variation at IL-4 to the immunopathogenesis of asthma, and propose that IL-4 might be useful as a genetic and immunological marker for both asthma susceptibility and phenotype stratification.