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Catecholamines up-regulate lipopolysaccharide-induced IL-6 production in human microvascular endothelial cells

Department of Surgery, University of Vienna, 1090 Vienna, Austria

¹Correspondence: Department of Surgery, University of Vienna, Währinger Gürtel 18–20, 1090 Vienna, Austria. E-mail: Michael.Bergmann{at}akh-wien.ac.at

The catecholamine-mediated modulation of the cytokine network has primarily been demonstrated for leukocytes. Whereas catecholamines decrease the LPS-induced production of IL-6 by leukocytes, serum levels of IL-6 are dramatically increased by the catecholamine epinephrine in animal endotoxemia models. We now demonstrate that epinephrine as well as norepinephrine can induce IL-6 in an endothelial cell line (HMEC-1). Furthermore, these catecholamines could even potentiate the LPS-induced IL-6 protein production. The synergistic effect of catecholamines and LPS could be reproduced in primary human skin microvascular endothelial cells. The catecholamine-induced IL-6 stimulation is based on increased IL-6 mRNA levels. RNA stability assays revealed that this regulation is not a result of enhanced RNA stability and therefore is most likely due to an increased transcription. Treatment with cycloheximide indicated that new protein synthesis is not necessary for this transcriptional up-regulation of IL-6 mRNA. Preincubation with and ß receptor antagonists showed that the effect is mediated by ß₁- and ß₂-adrenergic receptors. Thus, endothelial cells might be a possible source of increased IL-6 production observed in situations such as stress or septic shock, in which catecholamines are elevated due to endogenous production or exogenous application.—Gornikiewicz, A., Sautner, T., Brostjan, C., Schmierer, B., Függer, R., Roth, E., Mühlbacher, F., Bergmann, M. Catecholamines up-regulate lipopolysaccharide-induced IL-6 production in human microvascular endothelial cells.

Key Words: immunomodulation • transcription • adrenoreceptors

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