Bry K, Lappalainen U, Hallman M
Department of Pediatrics, University of California, Irvine 92717.
Biochim Biophys Acta. 1993 Mar 24;1181(1):31-6. doi: 10.1016/0925-4439(93)90086-g.
Proinflammatory cytokines may promote preterm labor in the setting of intrauterine infection. Tumor necrosis factor (TNF) and interleukin-1 (IL-1) synergistically stimulate the production of prostaglandin E2 (PGE2) by amnion cells. Transforming growth factor-beta (TGF-beta) inhibits the cytokine-stimulated PGE2 production. In the present study, we investigated the binding of IL-1 beta on human amnion cells in culture. Untreated amnion cells possessed 540 +/- 60 IL-1 receptors per cell, with a dissociation constant of 1.4 +/- 0.4 nM. Cells treated with TGF-beta 1 (10 ng/ml) had 570 +/- 110 receptors per cell. TNF-alpha (50 ng/ml) increased the number of IL-1 receptors to 2930 +/- 590. TGF-beta 1 inhibited the receptor upregulation by TNF-alpha. Cells treated with TGF-beta 1 and TNF-alpha expressed 1140 +/- 590 receptors per cell. The binding affinity was not changed by the cytokines. IL-1 receptor antagonist (IL-1ra) inhibited the stimulation of amnion cell PGE2 production by IL-1 beta, but not by TNF-alpha. Amnion cells secreted large amounts of IL-1ra (1.1 +/- 0.3 ng/10(5) cells). Treatment of the cells with TGF-beta 1 or TNF-alpha did not affect the release of IL-1ra. We conclude that IL-1 receptor expression is an important step in the regulation of the effects of cytokines on amnion cell PGE2 production.
促炎细胞因子可能在子宫内感染的情况下促进早产。肿瘤坏死因子（TNF）和白细胞介素-1（IL-1）协同刺激羊膜细胞产生前列腺素E2（PGE2）。转化生长因子-β（TGF-β）抑制细胞因子刺激的PGE2产生。在本研究中，我们调查了IL-1β与培养的人羊膜细胞的结合情况。未处理的羊膜细胞每个细胞有540±60个IL-1受体，解离常数为1.4±0.4 nM。用TGF-β1（10 ng/ml）处理的细胞每个细胞有570±110个受体。TNF-α（50 ng/ml）将IL-1受体数量增加到2930±590。TGF-β1抑制TNF-α引起的受体上调。用TGF-β1和TNF-α处理的细胞每个细胞表达1140±590个受体。细胞因子未改变结合亲和力。IL-1受体拮抗剂（IL-1ra）抑制IL-1β对羊膜细胞PGE2产生的刺激，但不抑制TNF-α的刺激。羊膜细胞分泌大量的IL-1ra（1.1±0.3 ng/10(5)个细胞）。用TGF-β1或TNF-α处理细胞不影响IL-1ra的释放。我们得出结论，IL-1受体表达是调节细胞因子对羊膜细胞PGE2产生影响的重要步骤。
