Reduction of plasma sCD40L and stimulated MIP-1-alpha production by in vivo beta-adrenergic stimulation

Abstract

Background: beta-Adrenergic receptor stimulation appears to have contrasting effects on inflammatory processes.

Methods: In 25 healthy volunteers we examined the effects of a 20-min isoproterenol infusion (20 ng/kg/min) on systemic and peripheral blood mononuclear cell (PBMC) production of LPS-stimulated inflammatory mediators.

Results: Plasma soluble CD40 ligand and stimulated MIP-1alpha production were both reduced (p < or = 0.05) by systemic beta-adrenergic stimulation. Stimulated TNF-alpha production was reduced (p < 0.03) but plasma TNF-alpha was unchanged. In contrast, plasma IL-6 was elevated (p < 0.05) while stimulated IL-6 was unchanged, indicating the main source may not be PBMCs.

Conclusions: beta-Adrenergic receptor activation leads to a reduction in markers of the early inflammation cascade. Our findings also suggest that adipose tissue is a contributing source of beta-adrenergically stimulated increases in circulating IL-6. Since beta-adrenergic agonists and antagonists are commonly used in the treatment of disease, it is important that we clearly elucidate and contrast their systemic versus cell-specific effects.