Activation of the humoral immune response in newborns` multiple organ failure syndrome is associated with the production of interleukin-1β, which is recognized via Toll-like receptors 2 (TLR2). The aim of this study was to determine the role of expression of the Toll-like receptors 2 gene in the pathogenesis of newborns with multiple organ failure syndrome. A prospective observational cohort study of 149 newborns was conducted. The main group (n = 113) were newborns with multiple organ failure syndrome, whereas the comparison group (n = 36) was newborns without this syndrome. The study included analysis of the expression of the TLR2 gene and its comparison with the concentration of interleukin-1β, peripheral blood lymphocyte count and clinical signs of the course of the disease. It was found that the population risk of reducing TLR2 expression was 79.33% in the main group, and 27.62% in the comparison group. Increasing the expression of the gene TLR2 in newborns leads to an increase in the concentration of interleukin-1β, an increase in the level of peripheral blood lymphocytes and is associated with the formation of microbial loci. Expression reduction of the TLR2 gene may lead to the development of multiple organ failure syndrome, systemic inflammatory response syndrome, increase in the number of affected organs, increased frequency of involvement in the immune system, and the need for aggressive respiratory therapy.

Keywords: multiple organ failure, newborn, toll-like receptor 2