PMID- 16095009 OWN - NLM STAT- MEDLINE DCOM- 20050830 LR - 20190911 IS - 0300-9742 (Print) IS - 0300-9742 (Linking) VI - 34 IP - 2 DP - 2005 Mar-Apr TI - Enhanced production of macrophage inhibitory protein-1alpha in patients with Behcet's disease. PG - 129-35 AB - 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 Behcet'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. CONCLUSION: 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. FAU - Kim, W U AU - Kim WU AD - Division of Rheumatology, Department of Internal Medicine, St. Vincent's Hospital, Seoul, Korea. FAU - Do, J H AU - Do JH FAU - Park, K S AU - Park KS FAU - Cho, M L AU - Cho ML FAU - Park, S H AU - Park SH FAU - Cho, C S AU - Cho CS FAU - Kim, H Y AU - Kim HY LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Scand J Rheumatol JT - Scandinavian journal of rheumatology JID - 0321213 RN - 0 (CCL2 protein, human) RN - 0 (Chemokine CCL2) RN - 0 (Chemokine CCL3) RN - 0 (Chemokine CCL4) RN - 0 (Chemokine CCL5) RN - 0 (Drug Combinations) RN - 0 (Interleukin-8) RN - 0 (Lipopolysaccharides) RN - 0 (Macrophage Inflammatory Proteins) RN - 0 (Phytohemagglutinins) RN - 56092-81-0 (Ionomycin) RN - NI40JAQ945 (Tetradecanoylphorbol Acetate) SB - IM MH - Adult MH - Aged MH - Behcet Syndrome/*blood/immunology MH - Blood Cells/drug effects/immunology MH - Cells, Cultured MH - Chemokine CCL2/blood MH - Chemokine CCL3 MH - Chemokine CCL4 MH - Chemokine CCL5/blood MH - Drug Combinations MH - Female MH - Humans MH - Interleukin-8/blood MH - Ionomycin/pharmacology MH - Lipopolysaccharides/pharmacology MH - Lymphocyte Activation/immunology MH - Macrophage Inflammatory Proteins/*blood MH - Male MH - Middle Aged MH - Phytohemagglutinins/pharmacology MH - Tetradecanoylphorbol Acetate/pharmacology EDAT- 2005/08/13 09:00 MHDA- 2005/09/01 09:00 CRDT- 2005/08/13 09:00 PHST- 2005/08/13 09:00 [pubmed] PHST- 2005/09/01 09:00 [medline] PHST- 2005/08/13 09:00 [entrez] AID - 10.1080/03009740410006943 [doi] PST - ppublish SO - Scand J Rheumatol. 2005 Mar-Apr;34(2):129-35. doi: 10.1080/03009740410006943.