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Results for “Complement Membrane Attack Complex”

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At least 1,225 records · Page 68Linked to original sources
PubMed1994

Susceptibility of C5b-9(m) to postmortem changes.

C5b-9(m) is a specific and sensitive marker for myocardial cell necrosis. The diagnostic value of this marker would be considerably limited in forensic practice if its immuno-histochemical demonstration were hampered by putrefaction or autolysis. We could demonstrate C5b-9(m) immunohistochemically in necrotic myocardium due to infarction up to the 11th day of experimentally induced putrefaction and autolysis, when reliable demonstration of myocardial infarction with hematoxylin-eosin was no longer possible. Under the experimental conditions of this study, no false positive immunohistochemical staining occurred.

Bias↗
PubMed1992

Protective effect of 16,16-dimethyl prostaglandin E2 on isolated rat hepatocytes against complement-mediated immune attack.

16,16-Dimethyl prostaglandin E2 was examined for its ability to inhibit complement-mediated in vitro hepatocytolysis by an antigen-antibody reaction. In the presence of fresh rat serum as a source of complement, 5-min culture of isolated rat hepatocytes with a monoclonal antibody against a rat liver-specific membranous antigen resulted in a marked, significant elevation in lactate dehydrogenase leakage into the culture medium. However, with heat-inactivated rat serum, such a reaction did not occur, indicating that the hepatocytolysis induced by the antibody was attributable to the membrane damaging action of complement activated by an antigen-antibody reaction. Pretreatment of the hepatocyte with 16,16-dimethyl prostaglandin E2 significantly suppressed the cytolytic reaction induced by the antibody in a concentration-dependent manner. These results show that 16,16-dimethyl prostaglandin E2 is capable of protecting isolated rat hepatocytes against the membrane-damaging insult of activated complement.

16,16-Dimethylprostaglandin E2↗
PubMed1993

Immunohistochemical alterations after muscle trauma.

The proteins fibrin, fibrinogen, fibronectin and complement C5b-9 were investigated in mechanically damaged skeletal muscle. An accumulation of fibrin, fibrinogen and fibronectin could be observed immediately after intra-vital trauma in damaged fibre zones, later an accumulation at the torn edges of the fibres. The accumulation of complement C5b-9 began one hour after trauma. After post mortem trauma no positive reactions could be observed for any of the proteins. The degree of expression of these proteins can therefore be used to differentiate between vital and postmortem muscle damage as well as the estimation of wound age in the early antemortem time period.

Animals↗
PubMed2000

Demonstration of myocardial necrosis in the presence of advanced putrefaction.

Samples of heart tissue were investigated in two series for the detectability of myocardial necrosis after artificial and natural putrefaction, respectively. In the first series heart tissue with and without infarction was artificially subjected to humid and dry autolysis and putrefaction. In the second investigation heart tissue was obtained from exhumed bodies after periods of burial ranging between 10 and 929 days. Besides histology a variety of immunohistochemical markers were applied and C5b-9 gave positive results even after long periods of artificial and natural putrefaction. From the methods tested, this was by far the most sensitive method with a high robustness against putrefaction. NP57, which indicates neutrophilic leucocytes could be demonstrated considerably longer after humid putrefaction than after dry putrefaction. The time limits of detection were considerably longer than for H&E. These two methods are the methods of choice for the detection of myocardial infarction and leucocyte infiltration in advanced stages of putrefaction.

Adult↗
PubMed2001

Aspects of our liver support systems using extracorporeal xenoperfusion of pig or baboon liver: review.

Artificial liver support systems using xenoperfusion of pig or baboon liver have metabolic activity and there is the possibility that they could substitute for total liver functions; however, several problems have yet to be solved. In our early clinical experience, a method of cross-hemodialysis with interposed cuprophane membrane was employed in order to avoid immunological reactions in patients. Sixteen patients with hepatic failure were treated by this method. Although the coma grade was ameliorated in 65% of the patients, the ultimate survival rate was 18.9%. In this clinical trial, the indication for liver support was clarified based on hepatic mitochondrial functions. This unsatisfactory result could also be attributed to insufficient effects of the device, due to the interposed membrane, and also to damage of the supporting livers due to hyperacute xenoperfusion injury. Recent investigations in the field of xenotransplantations have shown us possibilities for controlling xenogeneic hyperacute rejection. Suppression of complement activation enabled long-term xenoperfusion of supporting livers with high metabolic activity. The administration of prostaglandin E1 or soluble complement receptor type 1, and the use of transgenic pig livers expressing human decay-accelerating factor, may be promising methods to establish highly active artificial liver support systems using xenoperfusion.

Animals↗
PubMed1993

Calprotectin and complement activation during major operations with or without cardiopulmonary bypass.

Plasma concentrations of the granulocyte cell marker calprotectin were assessed during operation and 24 hours postoperatively in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass, abdominal aneurysmectomy with implantation of an aortic graft, or thoracotomy without implantation of synthetic material. The concentration of calprotectin increased significantly (p < 0.01) in all three groups. Ten of the 30 patients in the group undergoing cardiopulmonary bypass received methylprednisolone at the start of the operation. No difference in calprotectin concentration was seen between the two subgroups (p > 0.05). Plasma concentration of calprotectin was shown to increase rapidly in patients undergoing cardiopulmonary bypass and aneurysmectomy, in whom complement activation also took place. However, the calprotectin concentration increased slowly during the operation and the postoperative period in patients undergoing a thoracotomy, in whom complement was not activated. At wound closure the calprotectin concentration was significantly elevated in the cardiopulmonary bypass and aneurysmectomy groups compared with the thoracotomy group (p < 0.05). The calprotectin concentration remained elevated during the postoperative period in all three groups. Our results indicate that calprotectin may serve as a suitable cellular marker when the biocompatibility of artificial surfaces is studied.

Adult↗
PubMed1992

CD59 (homologous restriction factor 20), a plasma membrane protein that protects against complement C5b-9 attack, in human atherosclerotic lesions.

Blood cells express a cell membrane protein, termed homologous restriction factor 20 (HRF20) and identical to CD59, that can inhibit complement C5b-9 insertion into their membranes. In this report, we investigated by immunohistochemistry whether CD59 was present on cells in human atherosclerotic lesions since membranous C5b-9(m) has been found in lesions. Using a monoclonal anti-CD59 antibody, a cellular CD59 staining pattern was apparent in nearly all lesion specimens. CD59 stain co-localised with macrophage (CD14), T lymphocyte (CD7), endothelial cell (anti-factor VIII related antigen) and smooth muscle cell cytoskeletal-specific antigens (anti-alpha actin and muscle myosin). Endothelial cells always exhibited a more intense stain than the other cell types. CD59 antigen was not localised to any one area of the lesions. Usually CD59-positive cells occurred in clusters rather than as randomly spaced individual cells. CD59 did not stain all cells of the lesion and in particular did not appear to stain all smooth muscle cells. Areas of CD59-negative cells were sometimes observed to exhibit a cellular C5b-9 staining pattern. C5b-9 deposits were also observed in CD59-positive regions. Normal saphenous vein stained strongly for CD59 at the endothelial lining and weakly in the media. Capillaries in atherosclerotic intima always stained strongly for CD59. We conclude that HRF20 is constitutively expressed on endothelium and is under regulatory control in smooth muscle cells. Cellular C5b-9 attack in atherosclerotic lesions is therefore most likely to occur on smooth muscle cells.

Actins↗
PubMed1990

Cytotoxicity assays using cryopreserved target cells pre-labeled with the fluorescent marker europium.

We describe a method for standardizing cytotoxicity assays by the use of cryopreserved, fluorescently labeled target cells. The cells are labeled in batches with the fluorogenic element europium (Eu) and frozen in multiple aliquots. Replicate aliquots can be thawed on different days and used for cytotoxicity assays. Thawed pre-labeled cells from the same batch are killed reproducibly, allowing cytotoxicity assays to be standardized. The target cells need only be thawed, washed, counted for viability and used. The availability of pre-labeled, cryopreserved targets facilitates the assessment of cytotoxic activity of individual donors at different times. The method also simplifies the use of large panels of target cell types. By using this procedure it is not necessary to maintain active cultures of target cells, nor is it necessary to use and dispose of radioisotopes. These pre-labeled target cells can be used in various assays where the result is a destroyed target cell such as cell-mediated cytotoxicity, complement mediated cytotoxicity, or antibody-dependent cellular cytotoxicity.

Cell Survival↗
PubMed1991

Microparticle generation during in vitro platelet activation by anti-CD9 murine monoclonal antibodies.

We used flow cytometry and two anti-CD9 murine monoclonal antibodies (NNKY1-19, MALL13) to investigate the glycoprotein composition and the potential functions of microparticles (MP) released by platelets exposed to these antibodies in vitro. NNKY1-19 produced aggregation with characteristics similar to those noted in previous reports. The action of MALL13 on platelets in platelet-rich plasma (PRP), however, differs from that of other anti-CD9 antibodies. The normal fluctuation in the MALL13-induced change in optical density disappeared when complement was present. MALL13-induced effect for platelet in PRP was not inhibited by preincubation with monoclonal anti-GPIIb/IIIa antibody, but was inhibited in washed platelets (WP). Furthermore, following MALL13 stimulation in PRP platelets, the amount of buffer LDH markedly increased and electron microscopy findings showed vacuoles appearing inside the platelets. These results suggest that MALL13 has at least two effects on platelets that differ for PRP platelets and WP. The number of MP released was increased by the addition of anti-CD9 antibodies. MP surfaces were found to be rich in CD9 protein. MALL13 stimulation lead to a significant increase in the binding of C1q and C3 to platelets and caused the production of MP to occur more rapidly than it did the exposure of fibrinogen binding sites in the presence of complement. The analysis of the relationship of MP to anti-CD9 monoclonal antibody may be useful in the investigation of the relationship between platelet function and coagulation regulation.

Antibodies, Monoclonal↗
PubMed1992

Antigenic specificities of glomerular-bound autoantibodies in membranous glomerulopathy induced by mercuric chloride.

The present study describes the development of membranous glomerulopathy (MGP) with high proteinuria in DZB rats exposed to mercuric chloride (HgCl2). IgG1 and IgG2a antibodies, eluted from glomeruli with subepithelial immune deposits, bind to the interface of the GBM and epithelial cells. High reactivity to GBM was demonstrated by ELISA and Western blotting, which could be absorbed for 30% by laminin or laminin-associated extracellular matrix components. No reactivity was found with type IV collagen, fibronectin, heparan sulfate proteoglycans, or tubular brush border antigens. Absorption to GBM removed the reactivity to renal antigens. Passively transferred eluted antibodies bind in a predominantly linear pattern along the GBM, causing focal ultrastructural transformations of the podocytes. These results suggest that this type of HgCl2-induced MGP, associated with epithelial cell injury and proteinuria, is caused by autoantibodies to basement membrane components which are located at the epithelial cell-basement membrane interface and may be involved in cell-matrix binding.

Animals↗
PubMed1994

Effects of Ca2+ deregulation on mitochondrial membrane potential and cell viability in nucleated cells following lytic complement attack.

We have previously shown [Papadimitriou JC. Ramm LE. Drachenberg CB. Trump BF. Shin ML. (1991) J. Immunol., 147, 212-217] that formation of lytic C5b-9 channels on Ehrlich ascites tumor cells induced rapid depletion of adenine nucleotides associated with prelytic leakage preceding cell death. Extracellular Ca2+ concentration ([Ca2+]e) reduction by chelation markedly delayed the onset of cell death, although the adenine nucleotide leakage was enhanced. In the present study, we examined the temporal relationships between ionized cytosolic Ca2+ ([Ca2+]i), mitochondrial membrane potential (delta psi m) and cell death in individual cells by digital imaging fluorescence microscopy (DIFM), during the earliest phase of C5b-9 attack. The results showed an immediate, > 20-fold rise in [Ca2+]i, rapidly followed by dissipation of delta psi m and subsequent acute cell death. These events were markedly delayed by chelation of Ca2+e, but not by nominally Ca2+ free medium. Differing from previous reports indicating propidium iodide labeling of viable cells bearing C5b-9 channels, with DIFM we observed nuclear fluorescence with that marker only in association with cell death. These findings indicate that Ca2+ influx through lytic C5b-9 channels is responsible for the massive increase in [Ca2+]i, as well as for the rapid loss of delta psi m, followed by acute cell death. When this [Ca2+]i increase is prevented, the cell death is probably related to metabolic depletion.

Adenine Nucleotides↗
PubMed1995

Immunohistochemical detection of C5b-9(m) in myocardium: an aid in distinguishing infarction-induced ischemic heart muscle necrosis from other forms of lethal myocardial injury.

Immunohistochemical detection of C5b-9(m) is a reliable marker of very early cell necroses due to myocardial infarction. However, it is conceivable that it is also present in myocardial cell necroses caused by other types of hypoxic injury or by direct external trauma. If so, this would greatly limit the diagnostic value of C5b-9(m) in forensic practice. To clarify this issue, we performed immunohistological staining for C5b-9(m) in myocardium of 67 cases of 'direct' or possible 'indirect' myocardial injury not due to infarction.

Adult↗