Fieren M W, van den Bemd G J, Bonta I L, Ben-Efraim S
Department of Internal Medicine I, University Hospital Dijkzigt, Erasmus University Rotterdam, The Netherlands.
J Clin Lab Immunol. 1991 Jan;34(1):1-9.
We have reported previously that human peritoneal macrophages collected from patients on Continuous Ambulatory Peritoneal Dialysis (CAPD) during an episode of peritonitis secrete increased amounts of interleukin-1 (IL-1), as compared to those collected during an infection free period, provided the cells were stimulated in vitro by LPS. We now report that such macrophages release also higher amounts of Tumor Necrosis Factor (TNF), if collected during peritonitis and stimulated subsequently in vitro by LPS. The increase in release of TNF was ascertained by radio-immunoassays as well as by bioassay of cytostatic effect against the highly sensitive TNF target-cell line L929 murine transformed fibroblasts. The present reported results, in addition to previously reported data on release of IL-1, indicate that induction of release of cytokines from human peritoneal macrophages is a dual stepwise process: first priming in vivo in an inflammatory environment and, secondly stimulation in vitro by LPS.
我们先前曾报道，与在无感染期收集的人类腹膜巨噬细胞相比，在腹膜炎发作期间从持续非卧床腹膜透析（CAPD）患者身上收集的人类腹膜巨噬细胞，在体外经脂多糖（LPS）刺激后，会分泌更多的白细胞介素-1（IL-1）。我们现在报告，如果在腹膜炎期间收集此类巨噬细胞并随后在体外经LPS刺激，它们还会释放更高量的肿瘤坏死因子（TNF）。TNF释放的增加通过放射免疫测定以及对高度敏感的TNF靶细胞系L929小鼠转化成纤维细胞的细胞抑制作用生物测定来确定。除了先前报道的关于IL-1释放的数据外，本报告结果表明，人类腹膜巨噬细胞细胞因子释放的诱导是一个双步骤过程：首先在体内炎症环境中启动，其次在体外经LPS刺激。
