Differential involvement of sympathetic nervous system and immune system in the modulation of TNF-α production by α2- and β-adrenoceptors in mice

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In the present study, the regulation of tumor necrosis factor-α (TNF-α) production by α2- and β-adrenoceptors located on noradrenergic nerve terminals and on macrophages was studied in endotoxaemic mice. We found that reduction of the sympathetic outflow by reserpine dramatically increased the lipopolysaccharide (LPS)-induced TNF-α production, demonstrating that the release of endogenous noradrenaline (NA), controlled by presynaptic α2-adrenoceptors, was a determinant factor in this model. By using α2- and β-adrenergic drugs (clonidine, CH-38083, isoproterenol, propranolol) we provided the first in vivo evidence that, beside the dominance of neuronal α2- and macrophage β-adrenoceptors, the α2-adrenoceptors on macrophages were also involved in the modulation of LPS-induced TNF-α production. Since adrenergic drugs are widely used in the clinical practice, our findings may have therapeutical implications. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)34-40
Number of pages7
JournalJournal of Neuroimmunology
Issue number1
Publication statusPublished - Feb 1 2000



  • Cytokine
  • Endotoxaemia
  • Lipopolysaccharide
  • Neuroimmunomodulation
  • Noradrenaline
  • Sympathetic nervous system
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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