Soluble complement receptor 1 inhibits both complement and granulocyte activation during ex vivo hemodialysis.

J Himmelfarb, E McMonagle, D Holbrook, C Toth
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Abstract

Hemodialysis with cellulosic membranes results in both complement and granulocyte activation. We investigated the effects of soluble complement receptor 1 (sCR1), a potent complement inhibitor, on both complement and granulocyte activation in an ex vivo model of dialysis. Measurements were made of complement activation (radioimmunoassay for C3a desArg) as well as granulocyte activation (flow cytometric measurements of reactive oxygen species production, granulocyte CD11b/CD18 (MAC-1) expression and CD62L (L-selectin) expression). sCR1 completely abolished the generation of plasma C3a desArg during ex vivo hemodialysis. Without sCR1, C3a desArg levels rose from 968 +/- 373 ng/ml to 4961 +/- 40 ng/ml by the end of the ex vivo procedure (p < 0.001). sCR1 also completely inhibited MAC-1 upregulation and L-selectin shedding from granulocytes during ex vivo hemodialysis. With sCR1 there was still a statistically significant increase in granulocyte reactive oxygen species production (from 2.42 +/- 0.1 fluorescence channels to 6.47 +/- 0.7 fluorescence channels, p < 0.01) but a 50% inhibition when compared with experiments without sCR1 (3.15 +/- 0.5 to 11.2 +/- 1.9, p < 0.01). We conclude that sCR1 completely abolishes complement activation and changes in granulocyte cell adhesion molecules during ex vivo hemodialysis with cellulosic membranes. sCR1 partially inhibits granulocyte reactive oxygen species formation.

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可溶性补体受体1在体外血液透析过程中抑制补体和粒细胞的激活。
纤维素膜血液透析导致补体和粒细胞活化。我们在体外透析模型中研究了可溶性补体受体1 (sCR1),一种有效的补体抑制剂,对补体和粒细胞活化的影响。测量补体活化(C3a desArg的放射免疫测定)和粒细胞活化(流式细胞术测量活性氧产生、粒细胞CD11b/CD18 (MAC-1)表达和CD62L (l -选择素)表达)。体外血液透析过程中,sCR1完全消除血浆C3a desArg的产生。在没有sCR1的情况下,C3a desArg水平在离体过程结束时从968 +/- 373 ng/ml上升到4961 +/- 40 ng/ml (p < 0.001)。在体外血液透析过程中,sCR1也完全抑制MAC-1上调和l -选择素从粒细胞中脱落。添加sCR1后,粒细胞活性氧的产生仍有统计学意义的增加(从2.42 +/- 0.1荧光通道增加到6.47 +/- 0.7荧光通道,p < 0.01),但与不添加sCR1的实验相比,抑制了50%(3.15 +/- 0.5到11.2 +/- 1.9,p < 0.01)。我们得出结论,在纤维素膜离体血液透析过程中,sCR1完全消除补体活化和粒细胞粘附分子的变化。sCR1部分抑制粒细胞活性氧的形成。
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