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Increased circulating cytokine receptors and ex vivo interleukin-1 receptor antagonist and interleukin-1beta production but decreased tumour necrosis factor-alpha production after a 5-km run
Authors:JP Drenth  RJ Krebbers  J Bijzet  JW van der Meer
Affiliation:University Hospital St. Radboud, Nijmegen, The Netherlands. JPHDrenth@Compuserve.com
Abstract:
BACKGROUND: The purpose of this study was to examine the effect of a 5-km run on blood leucocytes, acute-phase proteins and cytokines. In addition, cytokines were measured in the supernatants from whole-blood cell cultures incubated with lipolysaccharide (LPS). METHODS: Ten healthy, recreational trained, athletes (three women, seven men) volunteered for this investigation. Samples were drawn just before, immediately after and at 3 h, at 24 h and at 48 h after the race. RESULTS: Exercise induced a transient leucocytosis (P = 0. 0002) and a mild acute-phase reaction with increase in plasma C-reactive protein (CRP) (P = 0.0115) but not in serum amyloid A (SAA) concentrations. Although plasma interleukin 6 (IL-6) was undetectable and soluble interleukin-1 receptor type II (IL-1sRII) remained unchanged, interleukin-1 receptor antagonist (IL-1ra) concentrations were elevated directly after the race with a further increase at 3 h (P < 0.0001). Soluble tumour necrosis factor (TNF) receptors were increased immediately after the run, but the effect was more marked for sTNFr p55 (two-fold increase; P < 0.0001) than for sTNFr p75 (1.16-fold increase; P = 00007). In cell cultures, the LPS-induced release of the inflammatory cytokines doubled for IL-1beta (P < 0.0001) and for IL-1ra (P < 0.0001). In contrast, TNF-alpha production decreased after the run, and a nadir was reached at 24 h (P < 0.0001). CONCLUSION: These results suggest that a 5-km run elicits both the production of acute-phase mediators (leucocytosis and elevation of CRP) and anti-inflammatory counter-regulation as judged by the increase in circulating concentrations of IL-1ra, sTNFr p55, and sTNFrp75 and down-regulation of LPS-stimulated TNF-alpha production.
Keywords:
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