Immunity and hemostasis system indicators in age groups of laboratory rats during the use of cyclosporine A

Abstract

Dysregulation of the T-cell link increases the susceptibility to cardiovascular disease with age. Therefore, we modeled immunosuppression and experimentally compared the state of the hemostasis system in young and old animals. White outbred male rats were used for the experiment. Cyclosporine in Sandimmun-Neoral (Novartis, Switzerland) was administered intramuscularly to experimental rats. Complement system proteins C3, C4, immunoglobulins (Ig) A, M, G and interleukin-6 were examined by enzyme immunoassay. Phenotyping of lymphocytes was performed by indirect immunofluorescence using monoclonal antibodies (subpopulations CD3+, CD19+, CD4+, CD8+, CD16+). The data obtained indicate that inhibition of the T-lymphocyte link (CD3+) does not necessarily lead to a compensated increase in the number of B-lymphocytes (CD19+), but stimulates their function: immunoglobulins are elevated (M, G). Under conditions of a reduced reaction from the cellular level, components of the complement system (C3, C4) are activated. Despite a slight decrease in phagocytic function, there was an increase in the number of natural killers (CD16+), active consumption of T-helpers (CD4+), a decrease in T-suppressors (CD8+), and an increase in the level of interleukin-6 in the plasma of experimental rats. Increased activity of antithrombin in old animals prevents procoagulant shifts against the background of excessive growth of "areas" with tissue factor. We found desquamated endotheliocytes, that opens the subendothelial layer and its level was higher in the experimental groups. Thus, we see an activation of the humoral link of the immune system. Experimental excessive concentration of the calcineurin blocker exposes the first pathogenetic links from the hemostasis system. An increase in the coagulation time of the initial stages of coagulation is combined with an acceleration of the final one. Despite the growth of fibrinogen in young animals, the mismatch in the regulation of the hemostasis system manifested itself mainly in old specimens of laboratory rats.