Membrane attack complex generation increases as a function of time in stored blood.
Membrane attack complex generation increases as a function of time in stored blood.
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DOI：
10.1111/tme.12109
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发表时间：
2014-04
期刊：
影响因子：
--
通讯作者：
Barnum SR
中科院分区：
文献类型：
--
作者：
Hu X;Patel RP;Weinberg JA;Marques MB;Ramos TN;Barnum SR
确定补体系统（一种有效的炎症介质）是否有助于红细胞储存期间的溶血。储存中的红细胞会发生结构和生化变化，可能导致输血后不良患者结局。白细胞耗竭和储存期间的补体激活可能导致红细胞储存损伤。我们通过ELISA对储存1至6周的去白细胞RBC单位等分试样进行了C3 a、C5 a、Bb、iC 3b、C4d和C5 b-9（MAC）水平的横断面分析。我们观察到，只有MAC水平显着增加红细胞单位作为存储时间的函数。我们还观察到，与RBC结合的C5 b-9的水平作为储存时间的函数而增加。膜攻击复合物水平随储存时间增加，表明MAC是储存RBC变化的主要补体介导因素。抑制终末补体途径可稳定RBC功能并延长保质期。
To determine if the complement system, a potent mediator of inflammation, contributes to hemolysis during RBC storage. Red blood cells in storage undergo structural and biochemical changes that may result in adverse patient outcomes post-transfusion. Complement activation on leukodepletion and during storage may contribute to the red blood cell storage lesion. We performed a cross-sectional analysis of aliquots of leukoreduced RBC units, stored for one to six weeks, for the levels of C3a, C5a, Bb, iC3b, C4d and C5b-9 (MAC) by ELISA. We observed that only MAC levels significantly increased in RBC units as a function of storage time. We also observed that the level of C5b-9 bound to RBCs increased as a function of storage time. Membrane attack complex levels increased over storage time, suggesting that MAC is the primary complement-mediated contributor to changes in stored RBCs. Inhibition of the terminal complement pathway may stabilize RBC functionality and extend shelf life.
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影响因子：
2.9
作者：
Gauvin, France;Spinella, Philip C.;Tucci, Marisa
通讯作者：
Tucci, Marisa
影响因子：
2.7
作者：
BLOMBACK, M;CHMIELEWSKA, J;AKERBLOM, O
通讯作者：
AKERBLOM, O
影响因子：
2.9
作者：
Kim-Shapiro DB;Lee J;Gladwin MT
通讯作者：
Gladwin MT
影响因子：
2.9
作者：
Weinberg, Jordan A.;Barnum, Scott R.;Patel, Rakesh P.
通讯作者：
Patel, Rakesh P.
DOI：
10.1084/jem.132.5.898
发表时间：
1970-11
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Götze O;Müller-Eberhard HJ
通讯作者：
Müller-Eberhard HJ