THE ROLE OF OPIOID RECEPTORS IN THE REGULATION OF PHAGOCYTOSIS AND THE PRODUCTION OF TH1/TH2 CYTOKINES UNDER ACUTE COLD STRESS IN NON-IMMUNE MICE

The endogenous opioid system plays an important role in the regulation of body functions under stress, providing stress-protective, analgesic and immunoregulatory effects. The aim of this work is to assess the effect of acute cold stress on the production of adaptive immunity cytokines IL-2, IL-4, IFN-γ, phagocytosis, and production of reactive oxygen species in non-immunized mice against the background of blockade of opioid receptors in vivo. The object of the study were male white mice that were subjected to acute cold stress at -20 C for 10 or 60 minutes. For the blockade of opioid receptors naloxone hydrochloride was used, which was administered subcutaneously at a dose of 0.2 mg/kg 20 min before stress. After exposure to stress, the spleen and peritoneal lavage were isolated from the animals. Сytokine concentrations were determined using ELISA. The absorption activity of CD11+ cells of the peritoneal cavity was assessed using FITC-stained St.cohnii on a flow cytometer, the production of reactive oxygen species was assessed using the reaction of luminol-dependent chemiluminescence. It was found that both experimental models naloxone independently inhibited the spontaneous production of IFN-γ. In stimulated cultures, an inhibitory effect on IFN-γ secretion was reported in animals subjected to only 60 min of stress, also independent of opioid receptor blockade. IL-2 production decreased in stimulated cultures against the background of 60 min stress naloxone independently. Both variants of cold stress had no effect on IL-4 production. Stress for 60 min inhibited absorption activity of CD11+ cells of the peritoneal lavage and activated production of oxygen radicals, which were canceled by the administration of naloxone. Thus, acute cold stress led to naloxone-independent inhibition of Th1 cytokine production by splenocytes, naloxone-dependent inhibition of phagocytosis, and activation of the microbicidal potential of peritoneal cavity cells.