医学
巨噬细胞移动抑制因子
滑液
痛风
关节炎
内科学
促炎细胞因子
痛风性关节炎
免疫学
外周血单个核细胞
细胞因子
骨关节炎
炎症
病理
体外
替代医学
化学
生物化学
作者
H.-R. Kim,K.-A. Lee,K.-W. Kim,B. Kim,S.-H. Lee
标识
DOI:10.1136/annrheumdis-2016-eular.1755
摘要
Background
Macrophage migration inhibitory factor (MIF) is proinflammatory, angiogenic and tissue degrading cytokine. Objectives
This study aimed to determine monosodium urate (MSU)-induced MIF production and the role of MIF in gouty arthritis. Methods
Peripheral blood and clinical data were obtained from 98 patients (31 patients with acute gouty arthritis and 67 patients with intercritical gout). Synovial fluid (SF) was obtained from patients with acute gouty arthritis and SF white blood cells and neutrophils were counted. SF and serum levels of MIF, interleukin (IL)-1, IL-8 and leukotriene B4, were measure using enzyme-linked immunosorbent assay (ELISA) and their relationship was analyzed. Peripheral blood mononuclear cells (PBMC) were isolated and cultured with MSU crystal, the production of MIF was determined. Results
SF MIF level was higher in acute gouty arthritis than osteoarthritis. Serum MIF was higher in patients with intercritical gout than patients with acute gouty arthritis or healthy volunteers. SF MIF level was positively correlated with SF WBC and neutrophil counts, IL-1b and IL-8 levels in acute gouty arthritis. Serum MIF level was correlated with IL-1b and IL-8 levels in patients with intercritical gout. MSU crystal induced MIF production in PBMC with maximal effect at 100mg/ml. Conclusions
MIF was highly produced in gouty arthritis and MSU induced MIF production. MIF could be involved in early inflammatory process in acute gouty arthritis. Acknowledgement
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology (NRF-2013R1A1A1008171). Disclosure of Interest
None declared
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