Interleukin-6 and Tumor Necrosis Factor-α Production After... : Biopsychosocial Science and Medicine (original) (raw)

ORIGINAL ARTICLES

Interleukin-6 and Tumor Necrosis Factor-α Production After Acute Psychological Stress, Exercise, and Infused Isoproterenol: Differential Effects and Pathways

Goebel, Marion U. MSc; Mills, Paul J. PhD; Irwin, Michael R. MD; Ziegler, Michael G. MD

From the Departments of Psychiatry (M.U.G., P.J.M., M.R.I.) and Medicine (M.G.Z.), University of California, San Diego, La Jolla, CA; Department of Medical Psychology (M.U.G.), University of Essen, Essen, Germany; and Veterans Affairs Medical Center (M.R.I.), La Jolla, CA.

Received for publication June 21, 1999;

revision received January 14, 2000.

Address reprint requests to: Marion Goebel, Department of Medical Psychology, Medical Faculty, University of Essen, Hufelandstr. 55, D-45122 Essen, Germany. Email: [email protected]

Abstract

Objective

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).

Methods

Thirty-two healthy volunteers performed speech and exercise tasks and underwent a 30-minute infusion of isoproterenol.

Results

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.

Conclusions

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.