Features of Immune System Disorders in Experimental Brain Trauma in Rats

Abstract

Introduction. Traumatic brain injury (TBI) is one of the common diseases of the person, which is accompanied by high mortality and disability of the victims. In the pathogenesis of TBI there are at least 2 periods that are associated with both primary nerve cell injury by the traumatic factor and secondary inflammatory-destructive changes that develop over a long period after the injury. An important role in the development of the second period of TBI is played by the body’s immune system, which can complicate the course of TBI and act differently depending on the severity of the injury.
 The goal of the work. The work investigated the state of proliferative and cytotoxic ability of splenocytes in light TBI in rats, which was caused by a drop in weight of 50 g from a height of 120 cm per animal.
 Materials and results. Studies have shown that within 24 hours after injury, there is an increase in the proliferative activity of splenocytes in the test for proliferation with mitogens, especially with KonA mitogen. While the cytotoxic activity of splenocytes is significantly inhibited at this time and the number of hyperdiploid cells in the spleen is reduced. At a later date after the injury, for 5 days, there is a significant recovery of immunological parameters, indicating that from the first hours after a mild TBI, the immune system changes in different directions, mainly towards the activation of proliferation, which may complicate the course the traumatic period.
 Conclusions. In experimental mild TBI, rats have differentiated changes in the activity of immune cells, which indicate the activation of the immune system in the early stages after injury.