Effects of stress on cytokine production

Physiologic stress results in significant alterations in the release of multiple cytokines. Increased production of interleukin-1 (IL-1) occurs following hemorrhage and thermal injury. Hemorrhage, accidental trauma and burns are followed by decreased interleukin-2 (IL-2) generation. Production of interleukin-3 (IL-3) and interleukin-5 (IL-5) is diminished following hemorrhage. Gamma-interferon release appears to be increased following hemorrhage. Stress secondary to infection is accompanied by marked elevations in serum levels of tumor necrosis factor (TNF), which contribute to hypotension and physiologic instability in this setting. Alterations in cytokine release probably play important roles in mediating alterations in immunologic, hemodynamic and cardiorespiratory function known to occur following physiologic stress. The production of all cytokines so far examined is altered by stress. Increased generation of IL-1, and probably of TNF and IL-6, contributes to the acute-phase reaction and hypermetabolic response which accompanies injury, burns, hemorrhage, and overwhelming infection. Severe immunosuppression, involving both T and B cell function, and contributing to the increased incidence of infection after injury may result, at least in part, from the multiple actions of stress-induced alterations in interleukin release. T cell activation is clearly affected by injury-induced decreases in IL-2, IL-3, and IFN-gamma release. Similarly, the depressed generation of systemic and mucosal antibodies to bacterial antigens following injury may be affected by alterations in the production of cytokines affecting B cell function, namely IL-1, IL-2, IL-3, IL-5 and IFN-gamma.(ABSTRACT TRUNCATED AT 250 WORDS)