[Neuroinflammation in the pathogenesis of central neuropathic pain]. / Neirovospalenie v patogeneze neiropaticheskogo bolevogo sindroma.

The problem of chronic pain is a significant question of nowadays medicine due to its high prevalence and treatment ineffectiveness in most cases. It has been proved by means of neuroimaging methods that chronic pain is always associated with glial activation in central nervous system, leading to the disturbance of glial cells participation in the eregulation of neuron microenvironment and neurotransmitter exchange. As a result, interneuronal communication in nociceptive pathways is interrupted and pathological neuroplasticity processes develop, causing the formation of pathological circuits, selfregilated by means of positive feedback. Thus, intervention that is directed to neuroinflammation suppression can by pathogeneticaly approved and effective method to treat chronic pain. In this review basic mechanisms of the inflammation initiation and maintaining in central nervous system in chronic pain are considered, pathological self-regulated circuits with neurons and immune cells are described and current chronic pain medications with antiinflammatiry and antinociceptive properties are listed.

[Biological activity of interferons in the novel coronavirus infection COVID-19].

INTRODUCTION: The immunopathogenesis of the novel coronavirus infection COVID-19 is usually associated with the development of imbalance in the immune response to its causative agent, SARS-CoV-2 virus (Coronaviridae: Coronavirinae: Betacoronavirus: Sarbecovirus). This is manifested, in particular, by interferons' (IFNs) deficiency at the beginning of the disease followed by hyperproduction of pro-inflammatory cytokines. The virus causes a decrease in IFN types I (α/ß) and III (λ) levels; changes in IFN type II (γ) are less studied. In this regard, it is relevant to assess the functional bioactive IFN (interferon status) in COVID-19. The aim of the study was to assess the antiviral potential of the body by testing the biologically active IFNs in COVID-19. MATERIAL AND METHODS: We used biological serum samples of COVID-19 patients taken in the acute phase (110 patients on the 1-5 days of the disease) and during rehabilitation (47 patients during 1-3 months after the disease onset). Assessment of interferon status was performed according to the technique developed by the authors and described earlier. RESULTS: The IFN status of patients with COVID-19 in the acute period and in the phase of post-infection rehabilitation was studied вduring the observation period. It was found that SARS-CoV-2 causes a pronounced inhibition of biological activity of IFN types I and II compared to the reference values by more than 20 and 7 times, respectively. During the post-COVID period, incomplete recovery of the IFN system activity was registered, which proceeded very slowly. No cases of reaching physiological indicators of interferon status were identified during the observation period. CONCLUSION: The obtained data on deficiency of the functional biologically active IFN confirm the hypothesis about the predominant role of impaired IFN production of different types in the immunopathogenesis of the novel coronavirus infection.