von Kempis J, Torbohm I, Schönermark M, Jahn B, Seitz M, Hänsch G M
Institut für Immunologie der Universität Heidelberg, FRG.
Int Arch Allergy Appl Immunol. 1989;90(3):248-55. doi: 10.1159/000235032.
We examined the prostaglandin E (PGE) synthesis of cultured adherent synovial fibroblast-like cells (SFC) from patients with osteoarthritis (OA) in the noninflammatory state as well as with rheumatoid arthritis (RA). In cells from RA patients the spontaneous PGE release was generally higher compared to that of OA patients, but decreased fast with time in culture. After cell passage, similar PGE baseline levels were seen in cells of the two patient groups. The cells could then be stimulated by the terminal complement components C5b-9 or C5b-8. PGE synthesis was also stimulated by the platelet-derived growth factor (PDGF), interleukin-1 (IL-1), or lipopolysaccharide (LPS). The amount of PGE synthesis after incubation with PDGF, LPS and IL-1 was comparable to that released after C5b-9. Thus, like other inflammatory mediators C5b-9 and PDGF trigger the increased PGE production by SFC and thus may participate in the development of synovial inflammation and contribute to the pathogenesis of RA.
我们检测了骨关节炎(OA)患者以及类风湿关节炎(RA)患者处于非炎症状态时培养的贴壁滑膜成纤维样细胞(SFC)的前列腺素E(PGE)合成情况。与OA患者的细胞相比,RA患者细胞的PGE自发释放通常更高,但在培养过程中随时间快速下降。细胞传代后,两组患者的细胞中可见相似的PGE基线水平。然后这些细胞可被终末补体成分C5b - 9或C5b - 8刺激。血小板衍生生长因子(PDGF)、白细胞介素 - 1(IL - 1)或脂多糖(LPS)也可刺激PGE合成。与PDGF、LPS和IL - 1孵育后的PGE合成量与C5b - 9作用后释放的量相当。因此,与其他炎症介质一样,C5b - 9和PDGF触发SFC增加PGE生成,从而可能参与滑膜炎症的发展并促成RA的发病机制。