Ransjö M, Marklund M, Persson M, Lerner U H
Department of Oral Cell Biology, University of Umeå, Sweden.
Arch Oral Biol. 1998 Apr;43(4):253-60. doi: 10.1016/s0003-9969(98)00010-7.
Prostaglandins are involved in force-induced orthodontic tooth movement. Bradykinin (BK) and thrombin are known to cause a significant time- and concentration-dependent burst of prostanoid biosynthesis in cultured human periodontal-ligament (PDL) cells. The aim now was to investigate interactive effects between interleukin 1 alpha, -beta (IL-1 alpha, -1 beta), tumour necrosis factor-alpha,-beta (TNF-alpha, -beta) and BK or thrombin on prostaglandin biosynthesis in human PDL cells. IL-1 alpha and -1 beta produced time- and concentration-dependent stimulation of prostanoid biosynthesis [prostaglandin (PG)E2 and 6-keto-PGF1alpha]. Synergistic stimulation of prostanoid biosynthesis was demonstrated when BK or thrombin were added together with IL-1 alpha or -1 beta. BK and IL-1 beta both significantly stimulated the release of [3H]arachidonic acid. No synergistic effect on [3H]arachidonic acid release was seen when BK and IL-1 beta were added simultaneously. These data suggest that the synergistic effect of BK and IL-1 beta on prostanoid biosynthesis is not due to interactions at the receptor level nor to enhanced release of arachidonic acid, but may be due to increased activity of cyclo-oxygenase. Also, TNF-alpha and -beta produced a concentration-dependent stimulation of PGE2 formation in cultured human PDL cells. Synergistic effects of BK and thrombin were demonstrated when PGE2 production was stimulated in combination with TNF-beta. In addition, a synergistic effect on the PGE2 response to IL-1 alpha or -1 beta was demonstrated when added in combination with TNF-alpha. These experiments demonstrate synergistic interactions between BK, thrombin, IL-1 and TNF on prostaglandin biosynthesis in cultured human PDL cells. The findings suggest that inflammatory mediators may act in concert in stimulating prostanoid production in response to pro-inflammatory stimuli. As an inflammatory reaction is seen in the periodontal ligament when teeth are orthodontically treated, this synergistic interaction may be of importance in force-induced tooth movement.
前列腺素参与了力诱导的正畸牙齿移动。已知缓激肽（BK）和凝血酶可在培养的人牙周膜（PDL）细胞中引起显著的时间和浓度依赖性前列腺素生物合成爆发。现在的目的是研究白细胞介素1α、-β（IL-1α、-1β）、肿瘤坏死因子-α、-β（TNF-α、-β）与BK或凝血酶之间对人PDL细胞中前列腺素生物合成的相互作用。IL-1α和-1β产生了时间和浓度依赖性的前列腺素生物合成刺激作用[前列腺素（PG）E2和6-酮-PGF1α]。当BK或凝血酶与IL-1α或-1β一起添加时，证明了对前列腺素生物合成的协同刺激作用。BK和IL-1β均显著刺激了[3H]花生四烯酸的释放。当BK和IL-1β同时添加时，未观察到对[3H]花生四烯酸释放的协同作用。这些数据表明，BK和IL-1β对前列腺素生物合成的协同作用不是由于受体水平的相互作用，也不是由于花生四烯酸释放的增加，而是可能由于环氧化酶活性的增加。此外，TNF-α和-β在培养的人PDL细胞中产生了浓度依赖性的PGE2形成刺激作用。当与TNF-β联合刺激PGE2产生时，证明了BK和凝血酶的协同作用。此外，当与TNF-α联合添加时，证明了对PGE2对IL-1α或-1β反应的协同作用。这些实验证明了BK、凝血酶、IL-1和TNF在培养的人PDL细胞中前列腺素生物合成方面的协同相互作用。研究结果表明，炎症介质可能协同作用，以响应促炎刺激而刺激前列腺素的产生。由于在正畸治疗牙齿时牙周膜中会出现炎症反应，这种协同相互作用可能在力诱导的牙齿移动中具有重要意义。
