title: Inhibition of lipopolysaccharide stimulated interleukin-1beta production after subarachnoid hemorrhage.
abstract: OBJECTIVE
  To identify the characteristics of cytokine production from peripheral blood mononuclear cells (PBMCs) in response to lipopolysaccharide (LPS) in patients with subarachnoid hemorrhage (SAH).
  
  
  METHODS
  Blood samples were collected on the first day and 3 days after SAH (n = 12) to measure plasma concentrations of catecholamines, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-10. PBMCs from SAH patients or healthy volunteers were incubated with LPS (1 microg) for 24 hours. In the second phase, PBMCs from healthy volunteers (n = 6) were incubated with or without catecholamine (10 micromol/1) for 6 hours. After pre-treatment, the cells were treated with LPS (1 microg) for 18 hours. Supernatants were extracted and subjected to measurement by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Plasma concentrations of epinephrine or dopamine prolong increased significantly 3 days after SAH, involved in elevation of plasma IL-10. In the PBMCs from the SAH patients, LPS-stimulated IL- 10 production was inhibited significantly. Pre-treatment with epinephrine or dopamine inhibited LPS-stimulated IL-1beta production significantly in the PBMCs from the healthy volunteers.
  
  
  CONCLUSIONS
  The initial SAH involved in an impaired production of pro-inflammatory cytokines in response to LPS with an elevation of plasma epinephrine, dopamine and IL-10 after acute stressful conditions. This phenomenon may play an important role of an early immnosupression in patients with poor grade SAH.
authors.affiliation: Department of Emergency and Critical Care Medicine, Nihon University School of Medicine, Tokyo 1738610, Japan. kosaku@med.nihon-u.ac.jp
authors.forename: Kosaku
authors.initials: K
authors.lastname: Kinoshita
authors.forename: Junko
authors.initials: J
authors.lastname: Yamaguchi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sakurai
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ebihara
authors.forename: Makoto
authors.initials: M
authors.lastname: Furukawa
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Tanjoh
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002395:Catecholamines / Q000097:blood / Q000494:pharmacology; D002478:Cells, Cultured; D004298:Dopamine / Q000097:blood; D015536:Down-Regulation / Q000187:drug effects / Q000276:immunology; D004660:Encephalitis / Q000097:blood* / Q000276:immunology* / Q000503:physiopathology; D004837:Epinephrine / Q000097:blood; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000276:immunology* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation / Q000187:drug effects / Q000276:immunology
chemical_list: D015415:Biomarkers; D002395:Catecholamines; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D004298:Dopamine; D004837:Epinephrine