Suppr超能文献

补体抑制和肝素涂层对人工表面诱导的白细胞和血小板活化的影响。

Effect of complement inhibition and heparin coating on artificial surface-induced leukocyte and platelet activation.

作者信息

Lappegård Knut Tore, Fung Michael, Bergseth Grethe, Riesenfeld Johan, Lambris John D, Videm Vibeke, Mollnes Tom Eirik

机构信息

Department of Medicine, Nordland Hospital, Bodø, and University of Tromsø, Tromsø, Norway.

出版信息

Ann Thorac Surg. 2004 Mar;77(3):932-41. doi: 10.1016/S0003-4975(03)01519-4.

Abstract

BACKGROUND

Exposure of blood to artificial surfaces, as in cardiopulmonary bypass, induces an inflammatory response involving complement, leukocyte and platelet activation. To elucidate the specific role of complement in this process, studies were performed on blood circulated in polyvinyl chloride tubing in the absence and presence of complement inhibitors. Parallel experiments were performed with heparin-coated polyvinyl chloride tubing, which is known to prevent complement and cell activation.

METHODS

A novel experimental model was used, based on human whole blood anticoagulated with lepirudin. Complement activation products, myeloperoxidase, lactoferrin, and thrombospondin were quantified in enzyme immunoassays. Leukocyte CD11b expression and leukocyte-platelet conjugates were detected by flow cytometry.

RESULTS

Increased levels of C3 activation products, alternative pathway convertase, and the terminal SC5b-9 complex, combined with unchanged levels of C1rs-C1-inhibitor complexes and marginal changes in C4 activation demonstrated that complement was activated through the alternative pathway. Granulocyte and monocyte CD11b expression and granulocyte-platelet conjugate formation were efficiently attenuated by blocking either factor D, C3, C5, or C5a receptor. In contrast, monocyte-platelet conjugate formation and release of myeloperoxidase, lactoferrin, and thrombospondin were not reduced by complement inhibition. Heparin-coated polyvinyl chloride tubing efficiently reduced all inflammatory markers studied, except for C1rs-C1-inhibitor complexes, which increased, consistent with the enhancing effect of heparin on C1-inhibitor function. This effect did not, however, reduce fluid-phase classic pathway activation induced by heat-aggregated immunoglobulin G.

CONCLUSIONS

Leukocyte and platelet activation in response to artificial materials occur by mechanisms that vary in their dependence on complement. Heparin coating precludes both the complement-dependent and complement-independent reactions.

摘要

背景

血液与人工表面接触,如在体外循环中,会引发涉及补体、白细胞和血小板激活的炎症反应。为阐明补体在此过程中的具体作用,我们对在有无补体抑制剂情况下在聚氯乙烯管中循环的血液进行了研究。同时,对已知可防止补体和细胞激活的肝素涂层聚氯乙烯管进行了平行实验。

方法

使用一种基于用重组水蛭素抗凝的人全血的新型实验模型。通过酶免疫测定法定量补体激活产物、髓过氧化物酶、乳铁蛋白和血小板反应蛋白。通过流式细胞术检测白细胞CD11b表达和白细胞 - 血小板结合物。

结果

C3激活产物、替代途径转化酶和终末SC5b - 9复合物水平升高,同时C1rs - C1抑制剂复合物水平未变以及C4激活仅有微小变化,表明补体通过替代途径被激活。通过阻断因子D、C3、C5或C5a受体可有效减弱粒细胞和单核细胞CD11b表达以及粒细胞 - 血小板结合物的形成。相比之下,单核细胞 - 血小板结合物的形成以及髓过氧化物酶、乳铁蛋白和血小板反应蛋白的释放并未因补体抑制而减少。肝素涂层聚氯乙烯管有效降低了除C1rs - C1抑制剂复合物外所有研究的炎症标志物,而C1rs - C1抑制剂复合物增加,这与肝素对C1抑制剂功能的增强作用一致。然而,这种作用并未降低热聚集免疫球蛋白G诱导的液相经典途径激活。

结论

对人工材料产生反应时白细胞和血小板的激活机制在对补体的依赖性方面存在差异。肝素涂层可防止补体依赖性和非补体依赖性反应。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验