Reperfusion injury of ischemic skeletal muscle is mediated by natural antibody and complement.
Reperfusion injury of ischemic skeletal muscle is mediated by natural antibody and complement.
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DOI：
10.1084/jem.183.5.2343
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发表时间：
1996-05-01
期刊：
影响因子：
--
通讯作者：
Carroll MC
中科院分区：
文献类型：
--
作者：
Weiser MR;Williams JP;Moore FD Jr;Kobzik L;Ma M;Hechtman HB;Carroll MC
缺血组织再灌注可引起急性炎症反应，导致局部血管内皮细胞和实质细胞的坏死和不可逆的损伤。为了研究缺血/再灌注损伤的发病机制，我们使用了缺乏补体成分C3、C4或血清免疫球蛋白的小鼠作为后肢缺血模型。我们发现，C3或C4纯合子缺陷的小鼠，基于显着减少放射性标记的白蛋白从血管系统泄漏出来，对再灌注损伤具有同等的保护作用。这表明经典途径补体是再灌流后炎症发生的重要因素。此外，血清免疫球蛋白缺乏的小鼠也同样受到保护，这种保护可以通过与正常小鼠的血清重组而逆转。因此，这份报告描述了一种新的再灌注损伤机制，涉及抗体沉积和补体激活导致炎症通透性。
Reperfusion of ischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient in C3 or C4 were equally protected against reperfusion injury based on a significant reduction in leakage of radiolabeled albumin out of the vasculature. This demonstrates that classical pathway complement is an important factor in the initiation of inflammation following reperfusion. Furthermore, mice deficient in serum immunoglobulin were equally protected and this protection could be reversed by reconstitution with serum from normal mice. Thus, this report describes a novel mechanism for reperfusion injury that involves antibody deposition and activation of complement leading to inflammation permeability.
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影响因子：
15.9
作者：
LEUNG, DYM;COLLINS, T;POBER, JS
通讯作者：
POBER, JS
DOI：
10.1073/pnas.87.7.2643
发表时间：
1990-04-01
影响因子：
11.1
作者：
VEDDER, NB;WINN, RK;HARLAN, JM
通讯作者：
HARLAN, JM
影响因子：
15.9
作者：
MA, XL;TSAO, PS;LEFER, AM
通讯作者：
LEFER, AM
影响因子：
64.8
作者：
MARKS, RM;TODD, RF;WARD, PA
通讯作者：
WARD, PA
DOI：
10.1073/pnas.92.25.11490
发表时间：
1995-12-05
影响因子：
11.1
作者：
WESSELS, MR;BUTKO, P;CARROLL, MC
通讯作者：
CARROLL, MC