Influence of Age and Immunostimulation on the Level of Toll-Like Receptor Gene (TLR3, 4, and 7) Expression in Foals

SIMPLE SUMMARY: Detailed knowledge of the molecular mechanisms of immunoglobulin synthesis appears necessary for a better understanding of foal immunity maturity and its influencing factors. At the same time, it encourages studies regarding the influence of the signaling cascade’s proteins on the primary immunological response, which provides an opportunity to develop extremely precise methods of regulating acquired immunity. The results revealed that the expression of theTLR3 and TLR4 genes, as well as the levels of immunoglobulins and interleukins, can be modulated by stimulation with the pharmacological agent, and that the expression of the TLR3 and TLR4genes in peripheral blood cells is dependent on age. ABSTRACT: The aim of this study was to investigate the molecular mechanisms leading to the identification of pathogens by congenital immune receptors in foals up to 60 days of age. The study was conducted on 16 foal Polish Pony Horses (Polish Konik) divided into two study groups: control (n = 9) and experimental (n = 7). Foals from the experimental group received an intramuscular duplicate injection of 5 mL of Biotropina (Biowet) at 35 and 40 days of age. The RNA isolated from venous blood was used to evaluate the expression of theTLR3, TLR4, and TLR7 genes using RT-PCR. The results of the experiment demonstrated a statistically significant increase in the level of TLR3 gene expression and a decrease in the level ofTLR4 gene expression with foal aging. The level of TLR7 gene expression did not show age dependence. Immunostimulation with Biotropina had a significant impact on the level of the genes’ expression for Toll-like receptors. It increased the level of TLR4 expression and decreased TLR3 expression. Thus, it was concluded that the expression of theTLR3 and TLR4genes in peripheral blood cells is dependent on age. This experiment demonstrated a strong negative correlation between TLR3 and TLR4 gene expression.