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PubMed1976

Role of complement components on cells and in cell interactions.

The complement system, though complex, is relatively easy to study both in terms of its reaction pathways, its distribution and its genetics. There is reason to believe that the complement system is involved in cell surface events and interactions at a variety of levels and we may hope that the knowledge of the system in the blood plasma will provide relatively easy insights into the more difficult areas with cells.

Antigen-Antibody Reactions↗
PubMed1981

Glomerular disease in two patients with urticaria-cutaneous vasculitis and hypocomplementemia.

We assessed the clinical, serologic, and renal abnormalities of two patients with the syndrome of hypocomplementemia, vasculitis, and urticaria. Both patients presented with recurrent urticaria and were found subsequently to have glomerulonephritis. Both manifested depletion of the early complement (C) components, and their Cl inhibitor levels were normal. Circulating immune complexes were detected by two of three assays in both patients. One patient had a high titer of Sm antibodies. The detectable immune complexes were of high molecular weight, and were more suggestive of classical lupus erythematosus than the low molecular weight (7S) Clq precipitins which characterize some cases of hypocomplementemia-vasculitis-urticaria syndrome. Biopsy of the skin lesions in both patients revealed leukocytoclastic vasculitis with immunoglobulin and C deposits at the dermal-epidermal junction. Renal biopsy specimens showed segmental or diffuse proliferative mesangial glomerulonephritis. The results suggest that patients with this syndrome do not conform to a discrete entity but rather exhibit a spectrum of diseases ranging from systemic lupus erythematosus to the syndrome of urticaria, hypocomplementemia, and low molecular weight Clq precipitins.

Adult↗
PubMed1998

Complement depletion improves neurological function in cerebral ischemia.

The contribution of the complement system to the exacerbation of cerebral ischemia/reperfusion injury was studied by comparing a group of rats with normal complement levels to another group that was complement depleted by cobra venom factor (CVF). The magnitude of reactive hyperemia was significantly greater in the complement depleted animals. There was also better preservation of somatosensory evoked potentials (SSEPs) in the complement depleted animals. These differences were not associated with changes in leukocyte infiltration as evidenced by myeloperoxidase and Leukotriene B4 activity. These data demonstrate that depleting the complement system can improve flow and outcome following cerebral ischemia with reperfusion.

Animals↗
PubMed1996

Pharmacological manipulation of the complement system in human diseases.

Complement is one of the powerful effector systems involved in the body's defense. When present in a dormant state it can, in concert with other components of immune system, protect the individual from foreign pathogens. However, inappropriately activated complement can cause disease. Several disease states such as immune complex and autoimmune diseases and deficiencies of some complement regulators are associated with inappropriate activation of complement. In some diseases complement is activated for a long or indefinite period while in others for a comparatively short time; in some it is activated systemically, in others locally; in some whole cascade is activated, in others only a few components are activated; in some classical pathway is activated, in others alternative pathway. In some diseases activation of complement takes place on cell and tissue surfaces. In many complement activating diseases biological activities of complement fragments become detrimental resulting in tissue injury and disease. Inhibition of complement by specific inhibitors is likely to arrest complement mediated disease processes. From this point of view, some laboratories are developing low molecular weight synthetic inhibitors whereas others are focusing on the development of high molecular weight plasma or cell surface complement inhibitors in their natural or recombinant forms for therapeutic purposes. A review concerning development of low molecular weight inhibitors with the eventual aim of manipulating complement system in human diseases was recently published (1,2). This review is concerned with high molecular weight natural or recombinant complement inhibitory molecules in human plasma or cell membranes, some of which are already in clinical use.

Autoimmune Diseases↗
PubMed1994

Complement activation and inhibition in myocardial ischemia and reperfusion injury.

The myocardial inflammatory response that occurs as a result of ischemia and reperfusion is similar to that which occurs in other tissues. Activation of the complement system is an integral part of the initiation and maintenance of any inflammatory response. It and other immune system mediators participate in the promotion of neutrophil adherence to endothelium by modulating expression of various adhesion molecules. The complement system also serves an integral role in mediating neutrophil activation, the results of which have been documented in the setting of myocardial ischemia and reperfusion. Another aspect of the complement cascade, which has received little attention with respect to the heart, is the direct effects of complement activation such as endothelial and myocardial cell cytotoxicity mediated by the membrane attack complex. It is likely that this form of tissue injury contributes significantly to myocardial reperfusion injury. Given the numerous contributions of the complement system to the generation of the inflammatory response, and to directly-mediated tissue injury, selective inhibitors of the complement system have great potential to limit reperfusion injury. This has already been demonstrated for the complement inhibitor sCR1. In the future, it is likely that any therapeutic treatment of reperfusion injury will include modulation of the effects of complement activation.

Animals↗
PubMed1975

Angioneurotic edema. A review of modern concepts.

We review the subject of angioneurotic edema with special emphasis on the more clearly defined entity of hereditary angioneurotic edema. The clinical presentations of the various forms of angioneurotic edema are discussed. Attention is directed toward the attempts that have been made to define this group of diseases in terms of their underlying biochemical mechanisms. A simplified schema of the serum complement system is presented. We conclude that only after we understand such biochemical interactions will we able to effect a more definitive form of therapy for the angioneurotic edemas.

Acute Disease↗
PubMed1997

Preventive role of lyophilic dairy products bulgaricum and biostim.

The purpose of the study was to examine the protective role of lyophilic dairy products bulgaricum and biostim with active bacteria lactic acid strain. Protective effect was determined as a phagocytosis activity and activity of major immunoglobulins. In total 120 men aged 30-35 years were included in three groups (30 controls with placebo). Daily doses (50 g) of these products were taken during a month. Positive responses from investigation links of immune system and paraspecific resistance were observed. Immunologic response was significantly higher after lyophilic dairy diet and this indicates that bulgaricum and biostim are products with protective role due to specific influence of bacteria lactic acid.

Adult↗
PubMed1998

Involvement of the complement system in antibody-mediated post-exposure protection against human immunodeficiency virus type 1.

We previously reported that passive transfer of a murine V3-specific monoclonal antibody (BAT123) to hu-PBL-SCID mice challenged with HIV-1LAI confers postexposure protection from infection. The role of the Fc fragment of this antibody as well as the involvement of the complement system in protection were evaluated in vivo. When we compared the postexposure protection offered by BAT123 and CGP 47439, a chimeric form of BAT123 in which the murine Fc domain has been replaced by a human IgG1 Fc domain, CGP 47439 failed to provide postexposure protection against HIV-1LAI despite having similar pharmacokinetics and in vitro neutralizing activity. Furthermore, when hu-PBL-SCID mice were treated with cobra venom factor, which inactivates serum complement activity, the postexposure protective ability of BAT123 was abrogated. These findings suggest that the complement system is involved in the passive protection against HIV-1 infection conferred by the murine monoclonal antibody BAT123 in hu-PBL-SCID mice.

Animals↗
PubMed1999

Cytotoxicity by stored human breast-milk: possible contribution of complement system.

Human milk stored over some period in vitro possesses certain cytotoxic properties, which require further studies. Cytolysis induced by stored human milk has now been further characterized, using rabbit red blood cells as targets, to determine the contribution of other components, particularly the complement system. Cytolysis was found to be temperature dependent, greatly enhanced by low concentrations of magnesium and calcium ions, but inhibited by moderate to excessive amounts of calcium ions, and by heating at 56 degrees C.

Animals↗
PubMed2003

Fibrillary glomerulonephritis with hypocomplementemia.

A 59-year-old man was referred for evaluation of nephrotic syndrome. The patient was diagnosed to have rheumatoid arthritis and had been treated for 10 years. Renal biopsy showed mesangial proliferation with small nodular formations, which were determined as fibrillary deposits (average diameter: 20 nm) by electromicroscopy. Congo-red stain was negative. The laboratory findings revealed hypocomplementemia and lambda type of Bence-Jones protein in urine without other systemic diseases including multiple myeloma. Immunosuppressive therapy did not attenuate the nephrotic-range proteinuria. Such a case of fibrillary glomerulonephritis with hypocomplementemia is rare.

Anti-Inflammatory Agents↗
PubMed2006

Clearance of apoptotic cells in human SLE.

Systemic lupus erythematosus (SLE) is characterized by a diverse array of autoantibodies, particularly against nuclear antigens, thought to derive from apoptotic and necrotic cells. Impaired clearance functions for dying cells may explain accumulation of apoptotic cells in SLE tissues, and secondary necrosis of these cells may contribute to the chronic inflammation in this disease. The exposure of phosphatidylserine (PS) and altered carbohydrates on dying cells are important recognition signals for macrophages. Furthermore, serum factors such as complement, DNase I, pentraxins (e.g. C-reactive protein) and IgM contribute to efficient opsonization and uptake of apoptotic and necrotic cells. Defects in these factors may impact the development of SLE in humans and mice in a variety of ways. We observed impaired clearance of apoptotic cells in lymph nodes and skin biopsies of humans with lupus, as well as intrinsic defects of macrophages differentiated in vitro from SLE patients' CD34+ stem cells, demonstrating that apoptotic cells are not properly cleared in a subgroup of patients with SLE. This altered mechanism for the clearance of dying cells may represent a central pathogenic process in the development and acceleration of this autoimmune disease.

Animals↗
PubMed2004

Improved suppression of circulating complement does not block acute vascular rejection of pig-to-rhesus monkey cardiac transplants.

At present, acute vascular rejection (AVR) remains a primary obstacle inhibiting long-term graft survival in the pig-to-non-human primate transplant model. The present study was undertaken to determine whether repetitive injection of low dose Yunnan-cobra venom factor (Y-CVF), a potent complement inhibitor derived from the venom of Naja kaouthia can completely abrogate hemolytic complement activity and subsequently improve the results in a pig-to-rhesus monkey heterotopic heart transplant model. Nine adult rhesus monkeys received a heterotopic heart transplant from wild-type pigs and the recipients were allocated into two groups: group 1 (n = 4) received repetitive injection of low dose Y-CVF until the end of the study and group 2 (n = 5) did not receive Y-CVF. All recipients were treated with cyclosporine A (CsA), cyclophosphamide (CyP) and steroids. Repetitive Y-CVF treatment led to very dramatic fall in CH50 and serum C3 levels (CH50 < 3 units/C3 remained undetectable throughout the experiment) and successfully prevented hyperacute rejection (HAR), while three of five animals in group 2 underwent HAR. However, the continuous suppression of circulating complement did not prevent AVR and the grafts in group 1 survived from 8 to 13 days. Despite undetectable C3 in circulating blood, C3 deposition was present in these grafts. The venular thrombosis was the predominant histopathologic feature of AVR. We conclude that repetitive injection of low dose Y-CVF can be used to continuously suppress circulating complement in a very potent manner and successfully prevent HAR. However, this therapy did not inhibit complement deposition in the graft and failed to prevent AVR. These data suggest that using alternative pig donors [i.e. human decay accelerating factor (hDAF)-transgenic] in combination with the systemic use of complement inhibitors may be necessary to further control complement activation and improve survival in pig-to-non-human primate xenotransplant model.

Animals↗
PubMed1992

The effect of systemic decomplementation with cobra venom factor on corneal complement levels in guinea pigs.

The authors examined the effect of systemic administration of cobra venom factor (CVF) on hemolytic complement levels in guinea pig sera and corneas. Guinea pigs received repeated intraperitoneal injections of CVF. Sera and corneas were obtained before and 1, 2, 5, 8, 10, 12, 16, and 20 d after the initial injection of CVF. Total hemolytic complement activity was measured by lysis of sheep erythrocytes sensitized with rabbit antibodies. There was a significant decrease in serum complement levels at days 1, 2, 5, 8, and 10 after the initial injection of CVF. After this, complement levels rose to levels that exceeded preinjection values. Complement levels in corneas also declined after CVF injections with a significant decrease at days 2, 5, 8, and 10 and a return to normal thereafter. Corneal complement depletion and restoration lagged behind serum. Moreover, the rate of complement depletion and restoration was greater for serum than cornea. Light microscopic examination of representative corneas at each time did not show local tissue changes during decomplementation. This is first study (to the authors' knowledge) to document corneal complement depletion by systemic administration of CVF. Low-to-absent corneal complement levels were present 2 d after the initial injection of CVF and persisted for 6 d. This model could be used to study the influence of complement on traumatic and immunologic injuries to the cornea.

Animals↗
PubMed1993

[Classification of urticaria and genetic angioedema].

Urticaria and genetic angioedema may be divided into three groups, according to their pathogenesis: anomaly of the complement system, physical origin or metabolic origin. Recent developments essentially concern hereditary angio-oedema, with location of the gene of the inhibitor of C1 esterase on chromosome 11 and the discovery of deletions or mutations of this gene in affected families.

Adult↗
PubMedDate not supplied

[Substances contained in the coelomic fluid of Lumbricus terristris having functions in common with those of some human complement components].

In the present work, it was demonstrated for the first time that the coelomic fluid of Lumbricus terrestris contained a substance recognized by human classical convertase. This substance permitted an immune, complement-dependent agglutination response of sheep erythrocytes carrying C3-convertase (EAC142). In addition, substances secreted by coelomic leukocytes possessed an inhibitory activity against human complement: the component C3 was cleaved into a C3b fragment. This result suggests the presence of a system the function of which is C3-convertase-like. We have thus shown that some complement functions, with their natural inhibitors, appear early in evolution. Certain of these functions and structures might be preserved throughout evolution.

Animals↗