title: 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.
authors.affiliation: Department of Psychiatry, UCSD Medical Center, University of California, San Diego, La Jolla, CA 92093-0804, USA. kmedwards@ucsd.edu
authors.forename: Kate M
authors.initials: KM
authors.lastname: Edwards
authors.forename: Suzi
authors.initials: S
authors.lastname: Hong
authors.forename: Barbara G
authors.initials: BG
authors.lastname: Woods
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Mills
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000328:Adult; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D023201:CD40 Ligand / Q000097:blood / Q000187:drug effects* / Q000276:immunology; D054405:Chemokine CCL3 / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood; D007545:Isoproterenol / Q000494:pharmacology; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D008875:Middle Aged; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000276:immunology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000187:drug effects
chemical_list: D000318:Adrenergic beta-Agonists; D015415:Biomarkers; C515429:CCL3 protein, human; D054405:Chemokine CCL3; D015850:Interleukin-6; D008070:Lipopolysaccharides; D011943:Receptors, Adrenergic, beta; D014409:Tumor Necrosis Factor-alpha; D023201:CD40 Ligand; D007545:Isoproterenol