Search results for "Complement Activation"
showing 6 items of 56 documents
Monoclonal antibodies against components of the classical pathway of complement.
1989
Activation of the classical pathway of complement involves several binding and enzymatic cleavage processes. Binding and enzymatic activation results in the appearance of new structures in the individual components. This report describes the different activation steps for C1q, C1r, C1s, C4 and C2 and summarizes monoclonal antibodies reported so far which recognize either conserved epitopes or activation-dependent epitopes with particular emphasis on neoepitopes occurring during the activation cascade.
Complement C6 deficiency protects against diet-induced atherosclerosis in rabbits.
1998
Abstract —Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non–C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment w…
Studies on the mechanism of PMN activation II. by triggering the alternative pathway of complement activation
1982
By means of cobra venom factor (CVF) it is demonstrated that the stimulation of hexosemonophosphate shunt (HMPS) of human polymorphonuclear leukocytes (PMN) by zymosan (Z) and dextran sulfate (DS) is caused by at least two modes of activation: (a) via activation caused by phagocytosis, (b) via activated alternative pathway of complement activation (APC). Active factors of APC presented with phagocytizable objects strongly enhance activation of PMN. The effect of APC can be observed in serum-containing as well as in serum-free cultures. It can be demonstrated that in serum-free cultures the factors of APC participating in the activation of PMN are supplied by monocytes. By the use of synthet…
Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rab…
1996
Objective: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex on infarct size, reflow and arrhythmogenesis. Methods: Twenty-eight C6-competent rabbits and 18 rabbits with congenital C6 deficiency were subjected to either 30 min or 2 h of coronary artery occlusion followed by reperfusion. C6 deficiency was confirmed by the complement titration test and immunohistology. The triphenyl tetrazolium chloride method was used to delineate infarct size. Reflow into infarcted areas was evaluated histologically afte…
Influence of cold ischemia time on complement activation, neopterin, and cytokine release in liver transplantation.
2004
The aim of this study was to determine whether a cold ischemia time (CIT) of12 hours influences the activation of complement as well as the plasma concentrations of neopterin, interleukin (IL)-6, or IL-8 in orthotopic liver transplantation (OLT).Eighteen consecutive patients undergoing OLT using a veno-venous bypass technique were divided into 2 groups: duration of CIT12 hours (group 1; n = 11), and CIT12 hours (group 2; n = 7). Blood samples were drawn preoperatively, 1 minute before, and 120 minutes after reperfusion.Preoperatively, complement split products, neopterin, IL-6, and IL-8 levels did not differ between the groups. At 120 minutes after reperfusion, the concentrations of C3a, SC…
Glucose-induced loss of glycosyl-phosphatidylinositol-anchored membrane regulators of complement activation (CD59, CD55) by in vitro cultured human u…
2000
Aims/hypothesis. This study examines whether increased glucose concentrations are responsible for a decreased expression of membrane regulators of complement activation molecules. The effect of high glucose in determining an increase in membrane attack complex deposition on endothelial cells was also investigated. Methods. Endothelial cells were isolated from umbilical cord tissue, cultured in the presence of increased concentrations of glucose, and the expression of CD46, CD55, and CD59 was detected by ELISA (enzyme-linked immunosorbent assay) and by flow cytometry. Glucose-treated endothelial cells were also incubated with antiendothelial cell antibodies and fresh complement to assess the…