Fujii I, Shingu M, Nobunaga M
Department of Clinical Immunology, Kyushu University, Beppu, Japan.
Ann Rheum Dis. 1990 Jul;49(7):497-503. doi: 10.1136/ard.49.7.497.
Monocytes from peripheral blood and synovial fluid of patients with definite and classic rheumatoid arthritis spontaneously produced significantly greater amounts of prostaglandin E2 (PGE2), leukotriene B4 (LTB4), and interleukin-1 beta (IL-1 beta) than samples of peripheral blood from normal controls. Peripheral blood monocytes from patients with rheumatoid arthritis produced significantly greater amounts of PGE2 than control samples when stimulated with lipopolysaccharide. There were no significant differences in the spontaneous release of superoxide or N-acetyl-beta-D-glucosaminidase by peripheral blood monocytes between patients and healthy controls. Both stimulated and unstimulated peripheral blood monocytes from patients with definite or classic rheumatoid arthritis produced significantly greater amounts of PGE2 than samples from normal controls. This was true, regardless of the stage of disease and the presence or absence of roentgenological joint abnormalities. Amounts of N-acetyl-beta-D-glucosaminidase released by peripheral blood monocytes from patients correlated positively with the erythrocyte sedimentation rate (ESR) and negatively with duration of disease. Amounts of IL-1 beta and N-acetyl-beta-D-glucosaminidase released from the peripheral blood monocytes of patients who had had their disease for less than one year were significantly higher than those of normal controls. There were no significant correlations between the types of treatment and the amounts of PGE2, LTB4, IL-1 beta or N-acetyl-beta-D-glucosaminidase released by peripheral blood monocytes in patients with rheumatoid arthritis. The findings suggest that monocytes are activated in patients with rheumatoid arthritis both at the onset of disease and during its chronic phase, and that they produce large amounts of mediators which may have a role in the induction and extension of the inflammatory process which leads to tissue damage.
确诊为典型类风湿性关节炎患者的外周血单核细胞和滑液单核细胞自发产生的前列腺素E2（PGE2）、白三烯B4（LTB4）和白细胞介素-1β（IL-1β）的量，显著高于正常对照者的外周血样本。类风湿性关节炎患者的外周血单核细胞在用脂多糖刺激后产生的PGE2量，显著高于对照样本。患者与健康对照者外周血单核细胞的超氧化物或N-乙酰-β-D-氨基葡萄糖苷酶的自发释放量没有显著差异。确诊或典型类风湿性关节炎患者的外周血单核细胞，无论是否受到刺激，产生的PGE2量均显著高于正常对照者的样本。无论疾病处于何种阶段以及是否存在X线关节异常，均是如此。患者外周血单核细胞释放的N-乙酰-β-D-氨基葡萄糖苷酶量与红细胞沉降率（ESR）呈正相关，与病程呈负相关。患病时间不足一年的患者外周血单核细胞释放的IL-1β和N-乙酰-β-D-氨基葡萄糖苷酶量，显著高于正常对照者。类风湿性关节炎患者接受的治疗类型与外周血单核细胞释放的PGE2、LTB4、IL-1β或N-乙酰-β-D-氨基葡萄糖苷酶量之间没有显著相关性。这些发现表明，类风湿性关节炎患者的单核细胞在疾病发作期和慢性期均被激活，并且它们产生大量介质，这些介质可能在导致组织损伤的炎症过程的诱导和扩展中起作用。
