活化的白细胞通过β2整合素/细胞间黏附分子-1机制与类风湿性关节炎的滑膜成纤维细胞相互作用后，表达并分泌巨噬细胞炎性蛋白-1α。
Activated leucocytes express and secrete macrophage inflammatory protein-1alpha upon interaction with synovial fibroblasts of rheumatoid arthritis via a beta2-integrin/ICAM-1 mechanism.
作者信息
Hanyuda M, Kasama T, Isozaki T, Matsunawa M M, Yajima N, Miyaoka H, Uchida H, Kameoka Y, Ide H, Adachi M
机构信息
Showa University School of Medicine, Tokyo, Japan.
出版信息
Rheumatology (Oxford). 2003 Nov;42(11):1390-7. doi: 10.1093/rheumatology/keg391. Epub 2003 Jun 27.
OBJECTIVE
To examine the expression and regulation of chemotactic factor, macrophage inflammatory protein-1alpha (MIP-1alpha) by fibroblast-like synoviocytes (FLS), monocytes and polymorphonuclear neutrophils (PMN) isolated from the synovial fluid (SF) of rheumatoid arthritis (RA) patients.
METHODS
Monocytes or PMN obtained from RA SF were co-cultured with unstimulated semiconfluent RA FLS. Culture supernatants were assayed for MIP-1alpha by enzyme-linked immunosorbent assay. The expression of MIP-1alpha mRNA and protein was also determined by Northern blot analyss and immunohistochemistry respectively.
RESULTS
Interaction of activated leucocytes with FLS synergistically increased MIP-1alpha expression and secretion via a mechanism mediated by beta2-integrin/ intercellular adhesion molecule 1.
CONCLUSION
MIP-1alpha expression within inflamed joints appears to be regulated not only by inflammatory cytokines but also by the physical interaction of activated leucocytes and FLS, and plays a crucial role in the progression and maintenance of RA synovitis.
目的
检测从类风湿关节炎（RA）患者滑液（SF）中分离出的成纤维样滑膜细胞（FLS）、单核细胞和多形核中性粒细胞（PMN）趋化因子巨噬细胞炎性蛋白-1α（MIP-1α）的表达及调控情况。
方法
将从RA滑液中获取的单核细胞或PMN与未受刺激的半汇合RA FLS共培养。采用酶联免疫吸附测定法检测培养上清液中的MIP-1α。分别通过Northern印迹分析和免疫组织化学法测定MIP-1α mRNA和蛋白的表达。
结果
活化白细胞与FLS相互作用，通过β2整合素/细胞间黏附分子1介导的机制协同增加MIP-1α的表达和分泌。
结论
炎症关节内MIP-1α的表达似乎不仅受炎性细胞因子调控，还受活化白细胞与FLS的物理相互作用调控，且在RA滑膜炎的进展和维持中起关键作用。
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