Tawara T, Shingu M, Nobunaga M, Naono T
Department of Clinical Immunology, Kyushu University, Japan.
Inflammation. 1991 Apr;15(2):145-57. doi: 10.1007/BF00917509.
The effects of recombinant human IL-1 beta on the production of prostaglandin E2 (PGE2), leukotriene B4 (LTB4), N-acetyl-beta-D-glucosaminidase (NAG), and superoxide by synovial cells and chondrocytes derived from osteoarthritis patients were determined. IL-1 beta markedly enhanced PGE2 production in chondrocytes and, to the lesser extent, in synovial cells. Synovial cells and chondrocytes spontaneously released LTB4 into culture medium and IL-1 beta significantly inhibited LTB4 production by these cells. IL-1 beta significantly suppressed the release of NAG and superoxide by synovial cells, whereas it significantly enhanced the production of NAG and superoxide by chondrocytes. Production of intracellular superoxide dismutase by synovial cells was significantly enhanced on incubation with IL-1 beta, but that of chondrocytes was not altered. IL-6, unlike IL-1 beta, significantly suppressed the production of NAG and superoxide by synovial cells and chondrocytes. These results suggest that IL-1 has differing effects on the release of mediators by synovial cells and chondrocytes and that these cells also vary in their responses to IL-1 beta and IL-6.
测定了重组人白细胞介素-1β(IL-1β)对骨关节炎患者滑膜细胞和软骨细胞前列腺素E2(PGE2)、白三烯B4(LTB4)、N-乙酰-β-D-氨基葡萄糖苷酶(NAG)以及超氧化物生成的影响。IL-1β显著增强软骨细胞中PGE2的生成,对滑膜细胞中PGE2生成的增强作用较小。滑膜细胞和软骨细胞可自发地将LTB4释放到培养基中,而IL-1β显著抑制这些细胞产生LTB4。IL-1β显著抑制滑膜细胞释放NAG和超氧化物,而显著增强软骨细胞中NAG和超氧化物的生成。滑膜细胞与IL-1β孵育后,细胞内超氧化物歧化酶的生成显著增强,但软骨细胞的超氧化物歧化酶生成未发生改变。与IL-1β不同,白细胞介素-6(IL-6)显著抑制滑膜细胞和软骨细胞产生NAG和超氧化物。这些结果表明,IL-1对滑膜细胞和软骨细胞介质释放具有不同影响,并且这些细胞对IL-1β和IL-6的反应也存在差异。