Cellular mechanisms of cold stress-related immunosuppression and the action of interleukin 1.

Recent studies of the immunomodulatory cytokines, especially interleukin 1 (IL-1), as the mediators of immunoneuroendocrine links have suggested their important physiological role in the development of host resistance during stress reaction. The present study examined the effects of cold stress (-20 degrees C, 20 min) in rats on the value of humoral immune response, lymphocyte activating factor (LAF) production by peritoneal macrophages, as well as IL-1 beta action on lymphocyte proliferation, and the level of general antibody titers. Cold stress exposure led to a considerable elevation of corticosterone (Cs) in rat blood serum and to pronounced suppression of humoral immune response. This kind of experimental stress induced peritoneal macrophages in rats to release LAF without additional stimulation within 24 h after termination of cooling. At the same time LAF production by macrophages after their additional stimulation by LPS in vivo and heat-killed staphylococcus in vitro was decreased during cold stress reaction. Cold stress exposure suppressed the ability of peripheral blood lymphocytes to proliferate in response to concomitant action of IL-1 beta. Immunoprotective effect of rat recombinant IL-1 beta administrated i.p. to rats before cooling was revealed. It is suggested that IL-1 beta modulates immunological and neuroendocrine responses to stress and plays a critical physiological role in realization of stress reaction.