Immunological parameters and gene polymorphisms (C-590T IL4, C-597A IL10) in severe bronchial asthma in children from the Krasnoyarsk region, West Siberia

Abstract

Background. Bronchial asthma is a common disease caused by interplay between multiple determinants, including genetic and immune variations. Objective. To investigate the main indices of humoral and cellular branches of immunity, features of cytokine regulation and cytokine genes in children with atopic bronchial asthma (BA) with different levels of disease control. Design. Fifty children with controlled BA (CBA) and 50 with uncontrolled BA (UBA) were analyzed. Mean age in the sample was 13.3692.24 years. A control group of healthy children (n=50) was also studied. All individuals were Russians (Eastern Slavs) from the Krasnoyarsk Territory, West Siberia. Diagnoses, severity and level of disease control were defined according to the Global Initiative for Asthma (GINA) recommendations. The lymphocytes were counted in blood using fluorescent microscopy. Humoral branch indices and cytokine levels (IL-2, IL-4, IL-10 and TNF-α) in blood serum were measured by ELISA. Genotyping of single-nucleotide polymorphism (SNP) in -590 position of the IL4 and -597 position of the IL10 gene was performed by restriction fragment length analysis. Results. No statistically significant differences in total IgE and cytokines blood levels were found in CBA and UBA. However, significant differences between the groups were found for CD3+, CD4+ and CD8+ cell counts. The T-590 allele of the IL4 gene, which is responsible for an increased serum level of IL-4, showed a tendency to an association with UBA. A decreased level of IL-10 enhances control over BA, which proves its association with the allelic variant A-597 IL10. Conclusions. Our data show that children with UBA have higher counts of CD3+ cells and an increase of sub-population of CD4+-cells as well as higher levels of IgE, IL-4 and TNF-α in blood serum as compared to CBA. Polymorphisms of the IL4 and IL10 genes are associated with allergic inflammation in UBA. © 2013 Marina V. Smolnikova et al.