Immune regulation in stress and emergency situations

Stress and emergencies significantly affect interactions between the central nervous system, endocrine pathways, and the immune system. Generally, it is assumed that stress-related HPA and sympathetic nervous system activity inhibits the functions of inflammatory cells, in particular IL-6 and TNF-α. In this context, modulation of the immune system is linked to infectious risk; furthermore, immune and endocrine parameters can be used in research objectively to proof effect of stress preventing and coping strategies. To investigate this, we measured effects of acute stress on several mediators with immune function, in addition to two hypothalamic-pituitary-adrenal axis hormones, and on serum noradrenaline (released in response to stimulation by sympathetic preganglionic neurons). The mediators with immune function included interleukin-6and tumor necrosis factor-α, leptin (which also acts as pro-inflammatory peptide), and somatostatin (which down-modulates a number of immune functions, such as lymphocyte proliferation, immunoglobulin production and the release of proinflammatory cytokines). The acute stress elicited increases in noradrenaline, ACTH, cortisol, IL-6, and leptin levels. Noradrenaline and ACTH exhibited the fastest and strongest stress responses, followed by cortisol, IL-6 and leptin. Furthermore, we could show in other studies that psychotherapeutic interventions for stress reduction induce changes in IgA and cortisol in saliva and allow verification of therapeutic success. Our data show that acute stress affects endocrine, immune andmetabolic functions in humans, and they show that mood plays a causal role in the modulation of responses to acute stress. This is a key to high susceptibility of people in situations of stress and emergencies.