The aim of the study was to assess the effects of three different methods of acute activation of the sympathetic nervous system on lipopolysaccharide-induced in vitro production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α).
Thirty-two healthy volunteers performed speech and exercise tasks and underwent a 30-minute infusion of isoproterenol.
As expected, acute activation of the sympathetic nervous system led to leukocytosis, including increases in lymphocyte, monocyte, and granulocyte populations (p values < .05). Lipopolysaccharide-induced IL-6 production was increased after both the speaking and exercise tasks (p values < .001), whereas TNF-α production was elevated only after exercise (p < .05). In contrast, infusion of isoproterenol inhibited TNF-α production (p < .001) and caused no change in IL-6 production.
In response to the challenges, IL-6 and TNF-α production showed different profiles. Purely β-agonist stimulation led to downregulation of TNF-α production, providing evidence of the antiinflammatory effect of in vivo β-receptor activation. The enhanced production of both cytokines after exercise, and of IL-6 after the speech task, can be best explained by a simultaneous upregulation of proinflammatory and inflammation-responding mediators. These effects may have an important role in controlling the immune response to acute psychological and physical stress.