Cellular,Molecular and Signaling Mechanisms in Neuro-Immune Interactions Under Stress

The role of Interleukin-1α/Interleukin-1β (IL-1α/IL-1β) production and blood levels, as well as ligand-receptor interactions of IL-1β with locating on immune and nerve target cells have been analyzed. Intracellular signal transduction via the sphingomyelin pathway during the development of stress reaction was also investigated. In mice stress of different durations and intensities induces an increase in the concentration of glucocorticoid hormones and IL-1α/IL-1β in blood. Thymocytes and lymphocytes responded to the concomitant actions of IL-1β, which correlated with the changes in the humoral immune response. These events coincided with stress-induced changes in the activity of neutral-sphingomyelinase, the key enzyme of the sphingomyelin cascade, in membrane fractions of both the mouse cerebral cortex and thymocytes. It is indicated that changes in functional activity of immune and nerve cells: e.g. proliferative activity of lymphocytes and thymocytes, cytotoxic activity of splenic natural killer (NK) cells, the intensity of cytokine signal transduction in the cells of the immune and neuroendocrine system, can define the disturbances in the immune system and the impairment of neural-immune interactions under stress.