Schmitz E, Ruschen S, Warnatz H
Department of Rheumatology and Clinical Immunology, Katholisches Krankenhaus Essen-Werden.
Z Rheumatol. 1987 Sep-Oct;46(5):227-32.
Peripheral blood monocytes (PBMo) and synovial fluid macrophages (SFMO) of patients with rheumatoid arthritis (RA), HLA B27-positive reactive oligoarthritis and controls were investigated for their capacity to generate superoxide anions (O2-) upon stimulation with phorbolmyristoacetate (PMA) in a cytochrome c (cyt c) microassay. PBMo of RA patients, patients with reactive arthritis and controls did not reveal any significant differences and also treatment of RA patients with gold salts or immunosuppressive therapy had no effect on the oxidative burst in PBMo. In contrast, in SFMO of RA patients treated only with nonsteroidal anti-inflammatory drugs (NSAID) we found significantly enhanced O2- release, compared with PBMo of the same group. Treatment with gold salts had no effect on this enhanced oxidative response, whereas immunosuppressive therapy with azathioprin or corticosteroids significantly reduced the O2- release of SFMO. In patients suffering from reactive arthritis we did not find significant differences between SFMO and PBMo. The O2- release of SFMO of this group was significantly reduced, when compared to that of SFMO of RA patients, treated with NSAID. These results indicated that SFMO but not PBMo in RA in cyt c microassay produce increased levels of activated oxygen species. In comparison to PBMo, SFMO of patients suffering from reactive arthritis do not show such an increased oxidative burst. These findings suggest that in RA, activated oxygen species have a local destructive effect in inflamed joints. This seems to be caused by activation of catalytic enzymes and complement components, as well as induction of release of interleukins or prostaglandins, contributing to the augmentation of the chronic inflammatory process.
采用细胞色素c（cyt c）微量分析法，研究了类风湿关节炎（RA）患者、HLA B27阳性反应性寡关节炎患者及对照者的外周血单核细胞（PBMo）和滑液巨噬细胞（SFMO）在用佛波醇肉豆蔻酸酯（PMA）刺激后产生超氧阴离子（O2-）的能力。RA患者、反应性关节炎患者和对照者的PBMo未显示出任何显著差异，用金盐或免疫抑制疗法治疗RA患者对PBMo中的氧化爆发也没有影响。相比之下，仅用非甾体抗炎药（NSAID）治疗的RA患者的SFMO中，与同一组的PBMo相比，我们发现O2-释放显著增强。金盐治疗对这种增强的氧化反应没有影响，而硫唑嘌呤或皮质类固醇的免疫抑制疗法显著降低了SFMO的O2-释放。在反应性关节炎患者中，我们未发现SFMO和PBMo之间有显著差异。与用NSAID治疗的RA患者的SFMO相比，该组SFMO的O2-释放显著降低。这些结果表明，在细胞色素c微量分析法中，RA患者的SFMO而非PBMo产生的活性氧水平升高。与PBMo相比，反应性关节炎患者的SFMO没有显示出这种增强的氧化爆发。这些发现表明，在RA中，活性氧在炎症关节中具有局部破坏作用。这似乎是由催化酶和补体成分的激活以及白细胞介素或前列腺素释放的诱导引起的，有助于慢性炎症过程的加剧。
