Cytokines' cascade changes in children with hearing loss depending on gap junction protein beta 2 (C.35delG) and interleukin 4 (C-590T) genes polymorphism
Larysa Sydorchuk, Oksana Iftoda, Andriy Sydorchuk, Oksana Kushnir, Ruslan Sydorchuk
The cytokines profile changes depending on genes mutations of connexin 26 (GJB2) (rs80338939) and interleukin 4 (IL-4) (rs 2243250) in children of Bukovina (West Ukraine) with sensorineural (SNHL) or conductive hearing loss (CHL) / deafness were evaluated. An imbalance of the immune response in children with SNHL characterized by inhibition of cellular Th1 immunity with Th2 humoral activation: genetically caused by low production of TNF-α and IL-1β in C-allele carriers of the IL-4 gene and low synthesis of IL-1β with high or normal synthesis of anti-inflammatory IL-4, IL-10 and IL-13 cytokines in mutant 36delG-genotype carriers of CJB2 gene and IL-4 hyperproduction in TT-genotype carriers of the IL-4 gene. CHL course in children is associated with an increase of TNF-α production (TT-genotype of IL-4 gene, p=0.02), which, however, was not enough to stimulate the synthesis of IL-1β, but caused direct compensatory hyperproduction of IL-4 (in T-allele carriers of IL-4 gene and in Non-del-allele carriers of CJB2 gene, p=0.002) with low production of IL-10 and IL-13 (in Non-del-allele carriers of CJB2 gene by 15.55% and 36.34%, p<0.05), confirming the presence of acute inflammation with cellular (mainly) and humoral (less) immune response activation.
How to cite this article:
Larysa Sydorchuk, Oksana Iftoda, Andriy Sydorchuk, Oksana Kushnir, Ruslan Sydorchuk . Cytokines' cascade changes in children with hearing loss depending on gap junction protein beta 2 (C.35delG) and interleukin 4 (C-590T) genes polymorphism. Pharma Innovation 2016;5(2):22-27.