title: Enhanced production of macrophage inhibitory protein-1alpha in patients with Behçet's disease.
abstract: OBJECTIVE
  Macrophage inhibitory protein-1alpha (MIP-1alpha), a C-C chemokine, stimulates the activation and migration of leukocytes. We investigated the expression of MIP-1alpha in patients with Behçet's disease (BD) and evaluated the association of the MIP-1alpha levels with disease activity of BD.
  
  
  METHODS
  Serum samples were obtained from 67 BD patients and 30 healthy controls. Simultaneously, whole blood cells were isolated from BD patients (n = 25) and healthy controls (n = 11) and cultured in the absence or presence of lipopolysaccharide (LPS), phytohaemagglutinin (PHA), and phorbol 12-myristate 13-acetate (PMA) plus ionomycin. The concentrations of MIP-1alpha, interleukin-8 (IL-8), regulated on activation, normally T cell expressed and secreted (RANTES), and monocyte chemoattractant protein-1 (MCP-1) were measured in the sera and culture supernatants by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  The serum levels of MIP-1alpha were higher in BD patients than in healthy controls. When whole blood cells were stimulated with LPS or PMA plus ionomycin, but not PHA, BD patients had higher levels of MIP-1alpha in the culture supernatants compared to healthy controls. In sera and culture supernatants of whole blood cells, MIP-1alpha levels correlated well with those of RANTES, MCP-1, and IL-8 in BD patients. Moreover, patients with active disease had significantly higher levels of serum MIP-1alpha levels compared with those with inactive disease.
  
  
  CONCLUSIONS
  MIP-1alpha levels were elevated in patients with BD, and correlated well with IL-8, RANTES, and MCP-1 levels. These results suggest that the increased MIP-1alpha levels in serum of BD patients may lead to activation and migration of leukocytes, playing a role, like other chemokines, in the pathogenesis of BD.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine, St. Vincent's Hospital, Seoul, Korea.
authors.forename: W U
authors.initials: WU
authors.lastname: Kim
authors.forename: J H
authors.initials: JH
authors.lastname: Do
authors.forename: K S
authors.initials: KS
authors.lastname: Park
authors.forename: M L
authors.initials: ML
authors.lastname: Cho
authors.forename: S H
authors.initials: SH
authors.lastname: Park
authors.forename: C S
authors.initials: CS
authors.lastname: Cho
authors.forename: H Y
authors.initials: HY
authors.lastname: Kim
mesh_terms: D000328:Adult; D000368:Aged; D001528:Behcet Syndrome / Q000097:blood* / Q000276:immunology; D001773:Blood Cells / Q000187:drug effects / Q000276:immunology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000097:blood; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000097:blood; D004338:Drug Combinations; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D015759:Ionomycin / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D004338:Drug Combinations; D016209:Interleukin-8; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D010835:Phytohemagglutinins; D015759:Ionomycin; D013755:Tetradecanoylphorbol Acetate