title: The effects of noradrenaline and alpha-2 adrenoceptor agents on the production of monocytic products.
abstract: There are some reports that catecholamines may modulate the production of monocytic cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF alpha). The present study was carried out in order to examine the effects of noradrenaline (10(-5), 10(-6) and 10(-7) M), clonidine (10(-5), 10(-6) and 10(-7) M), an alpha2-adrenoceptor agonist, and yohimbine (10(-5), 10(-6) and 10(-7) M), an alpha 2-adrenoceptor antagonist, on the production of IL-6, the IL-1 receptor antagonist (IL-1RA) and TNF alpha by stimulated whole blood of normal humans. We measured the in vitro production of IL-6, TNF alpha and IL-1RA by stimulated (phytohemagglutinin+lipopolysaccharide), diluted whole blood of 16 normal volunteers. The results show that noradrenaline, 10(-5) M, significantly suppressed the production of IL-6; noradrenaline, 10(-5) and 10(-6) M, significantly suppressed the production of IL-1RA and TNF alpha; clonidine, 10(-5) M, significantly suppressed the production of TNF alpha; and yohimbine, 10(-5) and 10(-6) M, significantly suppressed the production of IL-1RA. It is concluded that (1) noradrenaline has significant negative immunoregulatory effects in humans through suppression of the production of (monocytic) proinflammatory cytokines, e.g. IL-6 and TNF alpha, and (2) the suppression of the production of TNF alpha may be related to alpha(2)-adrenoceptor-related mechanisms.
authors.affiliation: Department of Psychiatry & Neuropsychology, University Hospital of Maastricht, P.O. Box 5800, AZ 6202 Maastricht, The Netherlands. crc-mh@online.be
authors.forename: M
authors.initials: M
authors.lastname: Maes
authors.forename: A
authors.initials: A
authors.lastname: Lin
authors.forename: G
authors.initials: G
authors.lastname: Kenis
authors.forename: B
authors.initials: B
authors.lastname: Egyed
authors.forename: E
authors.initials: E
authors.lastname: Bosmans
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D003000:Clonidine / Q000494:pharmacology; D005260:Female; D006801:Humans; D007108:Immune Tolerance; D007166:Immunosuppressive Agents / Q000378:metabolism; D066298:In Vitro Techniques; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D012795:Sialoglycoproteins / Q000096:biosynthesis* / Q000187:drug effects; D013315:Stress, Psychological / Q000276:immunology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000187:drug effects; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; C507763:IL1RN protein, human; D007166:Immunosuppressive Agents; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D015016:Yohimbine; D003000:Clonidine; D009638:Norepinephrine