Nishi K, Nishi O, Imanishi M
Nishi Eye Hospital, Osaka, Japan.
Nippon Ganka Gakkai Zasshi. 1993 Feb;97(2):156-61.
The authors proposed the hypothesis that pseudophakic inflammation, including the fibrin reaction, may be caused by interleukin (IL)-1, IL-6, other cytokines and/or prostaglandins (PGs), synthesized by residual lens epithelial cells (LEC). In testing our hypothesis, we have already detected IL-1 alpha, IL-6 and PGE2 in the culture media of human LEC obtained by capsulotomy during cataract surgery. In this paper, we studied the time course of PGE2-synthesis and interaction between IL-1 and PGE2. PGE2 concentration was measured by radioimmunoassay in the culture media to which rabbit antihuman IL-1 polyclonal antibody was added after culture for 6 h, 1 day, 1, 2, 3, 4, 5 and 6 weeks. There was no increase of PGE2, whereas in the untreated control culture media significant increase of PGE2 was confirmed. The results show that the antihuman IL-1 polyclonal antibody suppressed PGE2-synthesis. Thus, IL-1 induces PGE2 synthesis in human LEC culture.
作者提出一个假说,即包括纤维蛋白反应在内的人工晶状体炎症可能是由残留晶状体上皮细胞(LEC)合成的白细胞介素(IL)-1、IL-6、其他细胞因子和/或前列腺素(PGs)所引起。在验证我们的假说时,我们已经在白内障手术中通过截囊术获取的人LEC的培养基中检测到了IL-1α、IL-6和前列腺素E2(PGE2)。在本文中,我们研究了PGE2合成的时间进程以及IL-1与PGE2之间的相互作用。在培养6小时、1天、1、2、3、4、5和6周后,向培养基中加入兔抗人IL-1多克隆抗体,然后通过放射免疫测定法测量培养基中的PGE2浓度。PGE2没有增加,而在未处理的对照培养基中,PGE2有显著增加。结果表明,抗人IL-1多克隆抗体抑制了PGE2的合成。因此,IL-1在人LEC培养中诱导PGE2的合成。