Fieren M W, van den Bemd G J, Bonta I L
Department of Internal Medicine I, University Hospital Dijkzigt, Rotterdam, The Netherlands.
Prostaglandins Leukot Essent Fatty Acids. 1992 Sep;47(1):23-8. doi: 10.1016/0952-3278(92)90181-h.
In vitro secretion of the prostanoids PGE2 and PGI2 and of the cytokine IL-1 beta by peritoneal macrophages obtained from CAPD patients during episodes of peritonitis and infection free periods, was determined, after culturing with or without 5 micrograms/ml of LPS. The release of PGE2 and PGI2 as measured by its stable metabolite 6-keto-PGF alpha was determined in 10 episodes of peritonitis and 10 infection free periods. IL-1 beta release was determined in 14 episodes of peritonitis and 20 infection free periods. PGI2 release from macrophages declined sharply during peritonitis both in the absence and presence of LPS in the culture medium (p less than 0.005). A tendency to decreased PGE2 release was found during peritonitis, when macrophages were cultured in the absence of LPS. In the presence of LPS, the same amounts of PGE2 were released during peritonitis and during an infection free period. On the other hand, peritoneal macrophages released significantly more IL-1 beta during peritonitis as compared to an infection free period, provided that the cells were in vitro stimulated with LPS. In view of the interregulatory effects between prostanoids and macrophage cytokines in their production, these findings may indicate that the impaired release of PGI2 during peritonitis has allowed the macrophages to secrete more IL-1 beta after in vitro stimulation with LPS. This implies that PGI2 and PGE2 may play a distinct role in the regulation of cytokine secretion by these cells.
测定了在有或无5微克/毫升脂多糖(LPS)培养的情况下,从持续性非卧床腹膜透析(CAPD)患者腹膜炎发作期和无感染期获取的腹膜巨噬细胞中前列腺素PGE2和PGI2以及细胞因子IL-1β的体外分泌情况。通过其稳定代谢产物6-酮-PGFα测定PGE2和PGI2的释放量,在10例腹膜炎发作期和10个无感染期进行了检测。在14例腹膜炎发作期和20个无感染期测定了IL-1β的释放量。无论培养基中有无LPS,腹膜炎期间巨噬细胞释放的PGI2均急剧下降(p<0.005)。当巨噬细胞在无LPS的情况下培养时,腹膜炎期间发现PGE2释放有减少的趋势。在有LPS存在的情况下,腹膜炎期间和无感染期释放的PGE2量相同。另一方面,与无感染期相比,腹膜炎期间腹膜巨噬细胞释放的IL-1β显著更多,前提是细胞在体外受到LPS刺激。鉴于前列腺素和巨噬细胞细胞因子在产生过程中的相互调节作用,这些发现可能表明腹膜炎期间PGI2释放受损使得巨噬细胞在体外受到LPS刺激后能够分泌更多的IL-1β。这意味着PGI2和PGE2可能在这些细胞的细胞因子分泌调节中发挥不同的作用。