de Andres B, del Pozo V, Martin E, Palomino P, Lahoz C
Department of Immunology, Fundación Jimenez Diaz, Madrid, Spain.
Immunology. 1990 Feb;69(2):271-6.
Using an experimental model of mouse peritoneal eosinophilia, we investigated the role of Ca2+ in the in vitro activation of these cells challenged with specific Mesocestoides corti antigen. We have detected LTC4, a metabolite derived from arachidonic acid by way of 5'lipo-oxygenase and superoxide anion from the oxidative burst, as inflammatory mediators produced by activated eosinophils. Preincubation with hyperimmune mice serum increases the amount of LTC4 and superoxide anion in response to the antigenic extract. Release of O2- is inhibited by Verapamil (a voltage-gated calcium channel) and Quin 2 (an intracellular trapped chelator of calcium). Also, LTC4 produced by preincubated eosinophils challenged with M. corti is dramatically inhibited by Quin 2. Our results suggest an intact mechanism for calcium control for the release of these inflammatory mediators by eosinophils, after specific antigenic stimulation.
利用小鼠腹膜嗜酸性粒细胞增多症的实验模型，我们研究了Ca2+在体外激活受特定猬迭宫绦虫抗原攻击的这些细胞中的作用。我们检测到LTC4，一种通过5'-脂氧合酶从花生四烯酸衍生而来的代谢产物，以及来自氧化爆发的超氧阴离子，作为活化嗜酸性粒细胞产生的炎症介质。用超免疫小鼠血清预孵育会增加对抗抗原提取物时LTC4和超氧阴离子的量。维拉帕米（一种电压门控钙通道）和喹胺酸（一种细胞内捕获的钙螯合剂）可抑制O2-的释放。此外，喹胺酸可显著抑制经猬迭宫绦虫预孵育的嗜酸性粒细胞产生的LTC4。我们的结果表明，在特定抗原刺激后，嗜酸性粒细胞释放这些炎症介质的钙控制机制是完整的。
