Rasoul Nasiri1, Masoud Movahedi2, Ali Akbar Amirzargar3, Armin Hirbod-Mobarakeh4, Elham Farhadi5, Bita Ansaripour6, Batoul Moradi6, Nima Rezaei7. 1. Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran; Department of Pediatrics, Kurdistan University of Medical Sciences, Sanandaj, Iran. 2. Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. 3. Molecular Immunology Research Center; and Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: amirzara@tums.ac.ir. 4. Molecular Immunology Research Center; and Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. 5. Molecular Immunology Research Center; and Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Hematology Department, School of Allied Medical Science, Tehran University of Medical Sciences, Tehran, Iran. 6. Molecular Immunology Research Center; and Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 7. Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; Molecular Immunology Research Center; and Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: rezaei_nima@yahoo.com.
Abstract
OBJECTIVES: Allergic rhinitis (AR) is a polygenic inflammatory disorder of the nasal mucosa with an increasing prevalence worldwide. As interleukin 6 (IL-6) seems to be involved in development of allergic disorders, such as allergic rhinitis, this study was performed to evaluate the association of two promotor variants of IL-6 gene in the AR. METHODS: Ninety eight patients with AR were enrolled in this study. Genotyping was done for two polymorphisms in a promoter region of IL-6 gene (G/C at -174, rs1800795 and G/A at -597, rs1800797), using a PCR sequence-specific-primers method. RESULTS: Patients homozygous for the G allele of rs1800795 in IL-6 had a 3.35-fold risk of having AR than those with the C allele. AA genotype in rs1800797 of IL-6 was associated with the increased risk of developing AR. G/G haplotype for IL-6 (rs1800795, rs1800797) was significantly higher in the patient group. In some subgroups of patients, there were significant relationships between IgE levels, eosinophil count, eosinophil percentage, nature of sensitivity and persistency of disease and these two variants. CONCLUSION: We found that two promotor variants in IL-6, especially rs1800795, were predisposing factors for AR with a negative heterosis pattern. These SNPs could also affect the clinical parameters, the nature of sensitivity and persistency of the disease in some subgroups of the patients.
OBJECTIVES:Allergic rhinitis (AR) is a polygenic inflammatory disorder of the nasal mucosa with an increasing prevalence worldwide. As interleukin 6 (IL-6) seems to be involved in development of allergic disorders, such as allergic rhinitis, this study was performed to evaluate the association of two promotor variants of IL-6 gene in the AR. METHODS: Ninety eight patients with AR were enrolled in this study. Genotyping was done for two polymorphisms in a promoter region of IL-6 gene (G/C at -174, rs1800795 and G/A at -597, rs1800797), using a PCR sequence-specific-primers method. RESULTS:Patients homozygous for the G allele of rs1800795 in IL-6 had a 3.35-fold risk of having AR than those with the C allele. AA genotype in rs1800797 of IL-6 was associated with the increased risk of developing AR. G/G haplotype for IL-6 (rs1800795, rs1800797) was significantly higher in the patient group. In some subgroups of patients, there were significant relationships between IgE levels, eosinophil count, eosinophil percentage, nature of sensitivity and persistency of disease and these two variants. CONCLUSION: We found that two promotor variants in IL-6, especially rs1800795, were predisposing factors for AR with a negative heterosis pattern. These SNPs could also affect the clinical parameters, the nature of sensitivity and persistency of the disease in some subgroups of the patients.