Ward R A, Schmidt B, Blumenstein M, Gurland H J
Nephrology Department, Klinikum Grosshadern, University of Munich, Federal Republic of Germany.
Kidney Int. 1990 Feb;37(2):776-82. doi: 10.1038/ki.1990.45.
An ex vivo model of hemodialysis was used to evaluate the effect of dialysis membranes on phagocytic cell function. Blood was withdrawn continuously from healthy, non-uremic donors, heparinized, and pumped, single pass, through membrane modules under conditions which simulated normal dialysis conditions. The membrane modules contained membranes of cellulose, DEAE-substituted cellulose, or polysulfone. Blood was obtained from the module outlets for determination of complement activation, phagocyte elastase release, zymosan-induced phagocyte chemiluminescence, and monocyte interleukin-1 production. Significantly less complement activation occurred with the polysulfone and DEAE-substituted cellulose membranes than with cellulose membranes. Normal monocyte interleukin-1 production was not stimulated by any of the membranes used. In contrast, the cellulosic, but not the polysulfone, membranes primed the oxidative burst of the phagocytes and caused them to release elastase. DEAE-substituted cellulose had a lesser effect on elastase release than did cellulose and elastase release correlated significantly with the degree of complement activation. However, the correlation between complement activation and priming of phagocyte oxidative burst was weak, suggesting that membranes affect phagocyte oxidative metabolism through more than one mechanism. We conclude that some dialysis membranes stimulate the bacteriacidal functions of normal phagocytic cells, in part through complement-dependent mechanisms.
采用血液透析的体外模型来评估透析膜对吞噬细胞功能的影响。持续从健康的非尿毒症供体抽取血液,肝素化后,以单通道方式泵入模拟正常透析条件的膜组件。膜组件包含纤维素膜、二乙氨基乙基(DEAE)取代的纤维素膜或聚砜膜。从膜组件出口获取血液,用于测定补体激活、吞噬细胞弹性蛋白酶释放、酵母聚糖诱导的吞噬细胞化学发光以及单核细胞白细胞介素 -1 的产生。与纤维素膜相比,聚砜膜和 DEAE 取代的纤维素膜引发的补体激活明显较少。所用的任何一种膜均未刺激正常单核细胞白细胞介素 -1 的产生。相反,纤维素膜而非聚砜膜引发吞噬细胞的氧化爆发并使其释放弹性蛋白酶。DEAE 取代的纤维素对弹性蛋白酶释放的影响小于纤维素,且弹性蛋白酶释放与补体激活程度显著相关。然而,补体激活与吞噬细胞氧化爆发引发之间的相关性较弱,这表明膜通过多种机制影响吞噬细胞的氧化代谢。我们得出结论,一些透析膜部分通过补体依赖性机制刺激正常吞噬细胞的杀菌功能。