Frequency of Cytokine Gene Polymorphism in Full-Term Newborns with Hypoxic Events

Background. An infant brain damage is an extremely urgent problem, this pathology is difficult to prevent, and subsequently it manifests itself with a variety of neurological consequences. Various mechanisms are involved in neurodamage; cytokines, as well as genes that control their activity, are under a great concern today. However, there is little data about their role as predictors of the brain damage among children after hypoxia. Aim of the research. To identify the frequency of cytokine gene polymorphism: interleukin (IL)-1β(C-511T), IL-1β(C3953T), IL-4(C589T), IL-6(C174G), IL-10(C819T), IL-10(G1082A) among newborns with hypoxic events. Materials and methods. The study involved 128 full-term newborn patients with hypoxic events: the first group (n = 48) included newborns who experienced chronic intrauterine hypoxia (CVH), the second group (n = 80) included newborns born in asphyxiation. Control group (52) included babies born without asphyxia and not suffering from CVH. A retrospective analysis of case-records was carried out. The material for molecular genetic analysis was DNA samples isolated from umbilical cord blood leukocytes using DNA Express Blood reagents (Scientific and Production Company LITECH, Moscow). Results. Compared to the control group (p = 0.03) children born in asphyxia had their T allele IL-1β (C-511T) prevailed. The group of newborn who had CVH had their TT genotype (p = 0.04) and the T IL-1β allele (C-511T) (p = 0.01) prevailed compared to the control group. In the same study group while studying the polymorphism of the IL-1β gene, the T allele (p = 0.03) at the point C3953T prevailed, in contrast to the control group. Conclusion. Due to the fact that cytokines are part of a reaction cascade leading to the secondary brain damage, under the action of hypoxia, it was found that among newborns undergoing asphyxia and chronic intrauterine hypoxia the increased frequencies of carriage of IL-1β-511TT and IL-1β-3953TT genotypes, and IL-1β-511T and IL-1β-3953T alleles increase the risk of neurodamage.