title: RACK-1 expression and cytokine production in leukocytes obtained from AD patients.
abstract: OBJECTIVE
  The purpose of this study was to evaluate in vitro cytokine production in blood leukocytes obtained from sporadic AD patients, aged controls and young individuals.
  
  
  METHODS
  Diluted whole blood was treated in the presence or absence of LPS (1 microg/mL) for varying times (3-48 h). The release of IL-8, IL-10 and TNF-alpha in conditioned media was evaluated by commercially available sandwich ELISA.
  
  
  RESULTS
  Data obtained are indicative of the presence of an unregulated systemic inflammation in AD patients. Leukocytes obtained from AD patients had increased spontaneous TNF-alpha release and decreased LPS-induced IL-10 production, in comparison with both old controls and young subjects, while identical IL-8 production was observed in all groups. The last finding indicates that there was no shift in the potency or efficacy of the response towards LPS with aging, but alterations in downstream signal transduction pathways are probably altered with aging and pathological conditions.
  
  
  CONCLUSIONS
  The dysregulation of cytokine production observed in AD patients may partially be explained by a significant reduction in the expression of RACK-1, a protein crucial for integration of signaling pathways with different physiological functions, such as cytokine production.
authors.affiliation: Department of Experimental and Applied Pharmacology, University of Pavia, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Racchi
authors.forename: Elena
authors.initials: E
authors.lastname: Sinforiani
authors.forename: Stefano
authors.initials: S
authors.lastname: Govoni
authors.forename: Marina
authors.initials: M
authors.lastname: Marinovich
authors.forename: Corrado L
authors.initials: CL
authors.lastname: Galli
authors.forename: Emanuela
authors.initials: E
authors.lastname: Corsini
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000097:blood* / Q000235:genetics / Q000503:physiopathology*; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D019204:GTP-Binding Proteins / Q000032:analysis / Q000235:genetics* / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D016753:Interleukin-10 / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism*; D007962:Leukocytes / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis / Q000235:genetics* / Q000502:physiology; D000075370:Receptors for Activated C Kinase; D011956:Receptors, Cell Surface / Q000032:analysis / Q000235:genetics* / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D016209:Interleukin-8; D008070:Lipopolysaccharides; D009363:Neoplasm Proteins; C419368:RACK1 protein, human; D000075370:Receptors for Activated C Kinase; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D019204:GTP-Binding Proteins