Enhanced production of macrophage inhibitory protein-1α in patients with Behçet’s disease
- Author(s)
- W-U Kim; J-H Do; K-S Park; M-L Cho; S-H Park; C-S Cho; H-Y Kim
- Keimyung Author(s)
- Do, Ju Ho
- Department
- Dept. of Internal Medicine (내과학)
- Journal Title
- Scandinavian Journal of Rheumatology
- Issued Date
- 2005
- Volume
- 34
- Issue
- 2
- Abstract
- Objective: Macrophage inhibitory protein-1a (MIP-1a), a C–C chemokine, stimulates the activation and
migration of leukocytes. We investigated the expression of MIP-1a in patients with Behc¸et’s disease (BD) and
evaluated the association of the MIP-1a 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 (n525) and healthy controls (n511) 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-1a, 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 ofMIP-1a 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-1a in the
culture supernatants compared to healthy controls. In sera and culture supernatants of whole blood cells, MIP-1a
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-1a levels compared with those with inactive disease.
Conclusion: MIP-1a 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-1a 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.
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