NEURO-IMMUNE DISORDERS IN A MODEL OF POST-VIRAL CHRONIC FATIGUE SYNDROME. CORRECTION WITH RECOMBINANT IL-2 (RONCOLEUKIN)

Introduction Chronic fatigue syndrome is a severe chronic disease that leads to disruption of body systems. The lack of accurate diagnostic mechanisms makes it difficult to assess its prevalence, as well as to select an adequate treatment strategy. During the COVID-19 pandemic, the number of patients with symptoms of Chronic Fatigue Syndrome has sharply increased. There is a lot of evidence in the scientific literature that many infectious diseases can cause symptoms of this syndrome, for example influenza, enteroviruses. Neurological disorders in Chronic Fatigue Syndrome include memory problems, headaches, sleep disorders, unexplained joint and muscle pain, hypoactivation of the hypothalamus-pituitary-adrenal axis. The aim was to determine the possibility of correcting neuroinflammation and manifestations of fatigue/tiredness with a recombinant cytokine IL-2 preparation in rats under the Chronic Fatigue Syndrome model.

Methods. The study was performed on 50 male Wistar rats, the disease was modeled using a single intraperitoneal injection of Poly IC in a dose of 3 mg / kg of body weight of the animal. Half of the subjects were administered recombinant IL-2 (30 mg / kg) on the first day after the induction of the syndrome. On the 7th and 10th days of the experiment, motor activity, emotional status and the degree of physical fatigue were analyzed, after collecting the material, the concentration of lactate in the blood plasma, the degree of gene expression (IL-1β, IL10, INFα, 5HTT, TLR3) in the hypothalamus, as well as the activity of spleen lymphocytes (cytotoxic and proliferative activity), as a marker of immune system activity were determined.

Results. It was shown that a single administration of the recombinant cytokine IL-2 had a positive effect on the motor activity of experimental animals and normalized emotional reactions, reducing the level of anxiety-like behavior, restored the cytotoxic and proliferative activity of spleen lymphocytes, and prevented an increase in the expression of genes associated with inflammation. The exception was the TLR3 gene, the expression level of which did not decrease at all stages of the experiment, although positive dynamics were noted after the injection of recombinant IL-2.

Conclusion. The administration of the recombinant cytokine IL-2 to animals did not cancel the muscle weakness, it accelerated the normalization of physical activity and emotional status of animals, reducing manifestations of anxiety already on the 7th day of the experiment, and not on the 10th day, as in the group of rats that did not receive treatment.