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PubMed1993

Experimental studies of the influence of priming solutions on the systemic activation of complement during cardiopulmonary bypass: comparison between the use of albumin, hydroxyethyl starch and HWA-138.

Cardiopulmonary bypass surgery may be complicated by a systemic inflammatory reaction, which has been ascribed to activation of complement. For such activation, the choice of priming solution for the heart-lung machine may be of importance. The peripheral blood of three groups of eight donors was exposed to albumin, hydroxyethyl starch (HES) or to HWA-138 (pentoxifylline analogue) in addition to the priming solutions. The study confirmed that activation of complement is a consistent phenomenon during cardiopulmonary bypass surgery. The concentration of the C3 activation product C3a in the plasma was significantly increased after simulated extracorporeal circulation. However there were no differences within the increase of C3a concentrations between the various priming solutions.

Albumins↗

PubMed2004

Activation of the complement system generates antibacterial peptides.

The complement system represents an evolutionary old and significant part of the innate immune system involved in protection against invading microorganisms. Here, we show that the anaphylatoxin C3a and its inactivated derivative C3a-desArg are antibacterial, demonstrating a previously unknown direct antimicrobial effect of complement activation. The C3a peptide, as well as functional epitopes in the sequence, efficiently killed the Gram-negative bacteria Escherichia coli, Pseudomonas aeruginosa, and the Gram-positive Enterococcus faecalis. In mice, a C3a-derived peptide suppressed infection by Gram-positive Streptococcus pyogenes bacteria. Fluorescence and electron microscopy demonstrated that C3a binds to and induces breaks in bacterial membranes. C3a was also found to induce membrane leakage of liposomes. These findings provide an interesting link between the complement system and antimicrobial peptides, which are two important branches of innate immunity.

Amino Acid Sequence↗

PubMed2002

Transient leukopenia and anaphylatoxin production during granulocyte apheresis as treatment for ulcerative colitis.

It is well known that transient leukopenia due to activation of the alternative pathway of the complement system accompanies hemodialysis when cellulose acetate dialyzers are used. However, it has not been evaluated whether leukopenia also occurs during granulocyte apheresis (GCAP) as treatment for ulcerative colitis, in which an extracorporeal column is filled with cellulose acetate beads in order to remove circulating leukocytes. The aim of the present study was to evaluate whether transient leukopenia and activation of the alternative pathway of the complement system were observed during GCAP. In 8 patients undergoing GCAP weekly for 10 weeks, circulating leukocyte counts and plasma concentrations of C3a, a product of the activated alternative pathway of the complement system, were determined. GCAP elicited a rapid decline in the number of circulating leukocytes to 61.8 +/- 13.8% of the baseline value after 15 minutes of GCAP (P < 0.02). Thereafter, the number of circulating leukocytes returned to approximately baseline after 60 minutes. The baseline plasma C3a concentration was 123 +/- 61 ng/mL, and a significant increase to 425 +/- 123 ng/mL was observed after 15 minutes of GCAP (P < 0.02). The plasma C3a concentration reached 417 +/- 96 ng/mL after 60 minutes (P < 0.02). It thus follows that GCAP activates the alternative pathway of the complement system, resulting in anaphylatoxin production.

Adult↗

PubMed1995

Complement inhibition with an anti-C5 monoclonal antibody prevents acute cardiac tissue injury in an ex vivo model of pig-to-human xenotransplantation.

Prevention of hyperacute xenograft rejection in the pig-to-primate combination has been accomplished by removal of natural antibodies, complement depletion with cobra venom factor, or prevention of C3 activation with the soluble complement inhibitor sCR1. Although these strategies effectively prevent hyperacute rejection, they do not address the relative contribution of early (C3a, C3b) versus late (C5a, C5b-9) activated complement components to xenogeneic organ damage. To better understand the role of the terminal complement components (C5a, C5b-9) in hyperacute rejection, an anti-human C5 mAb was developed and tested in an ex vivo model of cardiac xenograft rejection. In vitro studies demonstrated that the anti-C5 mAb effectively blocked C5 cleavage in a dose-dependent manner that resulted in complete inhibition of both C5a and C5b-9 generation. Addition of anti-C5 mAb to human blood used to perfuse a porcine heart prolonged normal sinus cardiac rhythm from a mean time of 25.2 min in hearts perfused with unmodified blood to 79,296, or > 360 min when anti-C5 mAb was added to the blood at 50 micrograms/ml, 100 micrograms/ml, or 200 micrograms/ml, respectively. In these experiments, activation of the classical complement pathway was completely inhibited. Hearts perfused with blood containing the highest concentration of anti-C5 mAb had no histologic evidence of hyperacute rejection and no deposition of C5b-9. These experiments suggest that the activated terminal complement components C5a and C5b-9, but not C3a or C3b, play a major role in tissue damage in this porcine-to-human model of hyperacute rejection. They also suggest that targeted inhibition of terminal complement activation by anti-C5 mAbs may be useful in clinical xenotransplantation.

Acute Disease↗

PubMed1988

Complement conversion and leukocyte kinetics in open heart surgery.

Complement conversions and a pulmonary leukocyte sequestration were observed during cardiopulmonary bypass (CPB) in all of twenty patients who received open heart surgery. A systemic neutropenia was initially observed in the early phase of CPB, and it subsequently turned into a systemic neutrocytosis during the late phase of it. A significant leukocyte sequestration was found in the pulmonary circulation during CPB coincidently with the systemic neutropenia. The contribution of the transpulmonary sequestration to the leukopenia was major, being as high as 80 per cent. Plasma C3, C4, and CH50 levels rapidly decreased following the commencement of CPB. Alterations of the C3 molecule in the patients' plasma were demonstrated using the immunoblotting method. The appearances of C3a and C3b with the apparent molecular weights of 10,000 and 170,000 respectively, might be evidence of the complement activation during CPB. Another type of alteration in the C3 molecule was observed in the generation of a new fragment with the apparent molecular weight of 14,000. The appearance of this fragment, which did not share common epitopes with C3a, might suggest the consumption of complement components during CPB, unrelated to the activation of the complement systems.

Adult↗

PubMed1995

Toxicity of OKT3 increases with dosage: a controlled study in renal transplant recipients.

In the present study we prospectively compared side effects occurring in 12 patients after the first administration of low-dose OKT3 (0.5 mg twice daily) induction therapy with those in 10 patients who were treated with a conventional dose of OKT3 (5 mg daily) for acute rejection. We also investigated cytokine release and activation of complement and neutrophils as all of these are held responsible for OKT3-induced side effects. Low-dose OKT3 resulted in a significantly decreased side effects score compared to that after a conventional dose of OKT3 (1.8 vs 5.1, p = 0.0006). Following the first administration of low-dose OKT3, TNF peak levels were significantly lower than after a conventional dose of OKT3. In contrast to our data on conventional dose OKT3 treatment, the first administration of low-dose OKT3 did not induce complement activation as reflected by C3a and C4b/c levels in plasma. Finally, the increase in neutrophil degranulation products lactoferrin and elastase-varies; is directly proportional to 1-antitrypsin was much less following 0.5 mg OKT3 than following 5 mg. We conclude that OKT3-induced toxicity is dose-dependent and is mediated not only by cytokine release but also by activation of complement and neutrophils.

Dose-Response Relationship, Drug↗

PubMed1999

Complement activation in patients with systemic lupus erythematosus without nephritis.

OBJECTIVE: To study the association between disease activity and complement activation prospectively in patients with systemic lupus erythematosus (SLE). PATIENTS AND METHODS: Twenty-one SLE patients were examined monthly for 1 yr. Disease activity, autoantibodies, conventional complement tests and the following complement activation products were investigated: C1rs-C1inh complexes, C4bc, Bb, C3a, C3bc, C5a and the terminal SC5b-9 complement complex (TCC). RESULTS: Modest variation in disease activity was noted. None of the patients had nephritis. Flare was observed at 27 visits. Four patients had anti-C1q antibodies in conjunction with modestly low C1q concentrations. The complement parameters were rather constant during the observation period. Slightly to moderately decreased C4 (0.05-0.10 g/l) was found in 10 patients and severely decreased C4 (<0.05 g/l) in seven patients. Decreased C4 was not associated with increased complement activation. Complement activation products were either normal or slightly elevated. TCC was the only activation product correlating significantly with score for disease activity at flare. None of the variables tested predicted flares. CONCLUSION: Complement tests are of limited importance in routine examination of SLE without nephritis, although TCC is suggested to be one of the most sensitive markers for disease activity.

Adult↗

PubMed1990

Clinical and experimental approaches to the prevention of atherosclerosis by immunological regulations.

To evaluate the involvement of the complement system in atherogenesis, we investigated the effect of camostat mesilate (CM), C1r, and C1 esterase inhibitor on cholesterol-induced atherosclerosis in rabbits. We also examined the effect of sodium dextran sulfate (DS, molecular weight: 7000), which is reported to be effective in preventing arteriosclerotic diseases and in inhibiting cholesterol-induced atherosclerosis in experimental animals, on complement activation in vitro and in vivo. The administration of CM reduced the formation of atherosclerotic lesions in cholesterol-fed rabbits. DS inhibited complement pathway in vitro, and the administration of DS reduced the C3a level in subjects. These results suggest that complement activation may possibly be involved in the atherosclerotic process.

Aged↗

PubMed1997

Inhibition of complement activation by soluble recombinant CR1 under conditions resembling those in a cardiopulmonary circuit: reduced up-regulation of CD11b and complete abrogation of binding of PMNs to the biomaterial surface.

The influence of soluble recombinant CR1 (sCR1) on complement activation, and its indirect effects on the coagulation system and cellular responses were assessed in two models for the study of blood/surface and blood/air interactions, as are encountered in e.g. cardiopulmonary bypass circuits. The concentrations of C3a and sC5b-9 and the amount of bound C3/C3 fragments were analyzed as indicators of complement activation. Thrombin-antithrombin complexes, the platelet count, surface-ATP, beta-thromboglobulin, and the expression of CD11b on leukocytes were the parameters analyzed to reflect coagulation and cellular responses. In addition, immunochemical analyses of the phenotypes of surface-bound leukocytes and platelets were performed. Recombinant sCR1, at doses ranging between 0.1-0.25 mg/ml, was found to completely inhibit the generation of sC5b-9, and of C3a by two thirds; the binding of C3 and/or C3 fragments to the surface was almost entirely abolished. As a result of the inhibition of complement activation, the expression of CD11b on PMNs, and the binding of these cells to the biomaterial surface was almost completely lost. In contrast, the thrombin-antithrombin complexes, the platelet count, and the adherence of platelets to the surface, as reflected by the ATP binding and the release of beta-thromboglobulin, were not affected. These data show that complement activation, in association with extra-corporeal treatment, causes activation and binding of PMNs to the biomaterial and that these effects can be completely abolished by the addition of soluble recombinant sCR1.

Biocompatible Materials↗

PubMed1988

The effects of complement activation during cardiopulmonary bypass. Attenuation by hypothermia, heparin, and hemodilution.

Complement activation was examined prospectively in 100 cardiopulmonary bypass (CPB) patients. Plasma C3a desArg (C3a) increased (cannulation: 234 +/- 33 ng/mL; 20 minutes on CPB: 622 +/- 51; 2 hours after CPB: 1143 +/- 109, p less than 0.0001). C3a at 2 hours was higher in the 13 patients requiring mechanical ventilation for longer than 1 day (1023 +/- 274) than in the 67 without respiratory complication (568 +/- 45, p less than 0.004). Five more patients were studied for neutrophil activation to confirm that a biologic effect of complement activation occurs during CPB; in these five patients C3a increased to 317% of baseline after 10 minutes on CPB with a corresponding rise in neutrophil cell surface receptors for the complement opsonin C3b (as measured by indirect immunofluorescence) to 168% (p less than 0.05). Both increases were sustained at 30 minutes. Temperature, dilution, and heparin were studied as variables relevant to CPB. Exposure of normal neutrophils to C5a in vitro caused an increase in C3b receptors which was dependent on temperature (0 specific fluorescence at 0 C, 30 at 25 C, 180 at 30 C, and 275 at 37 C). Generation of C3a and C5a in normal serum by zymosan was also temperature-dependent (ng/mL C5a generated: 0.7 at 25 C, 200 at 30 C, and 897 at 37 C; ng/mL C3a generated: 546 at 25 C, 10,872 at 30 C, and 65,667 at 37 C). Serum dilution to 33% decreased ng/mL C5a generated in the same system from 200 to 76 with no effect on C3a. Addition of heparin to 20 U/mL decreased ng/mL C3a generated from 10,872 to 913 and C5a from 200 to 8. Thus, hypothermia, dilution, and heparin protect CPB patients from complement activation by reducing both generation of C3a/C5a and the subsequent cellular response of neutrophil activation.

Cardiopulmonary Bypass↗

PubMed1996

Cytokine production during hemodialysis: effects of dialytic membrane and complement activation.

Interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are closely associated with acute and chronic inflammatory processes in hemodialytic patients. However, the mechanisms concerning cytokine production by monocytes during hemodialysis are still conflicting. With the use of the more specific monoclonal antibody ELISA method, contamination detection and crossover protocol of complement-activating and noncomplement-activating hollow fibers, we were able to confirm augmented II-1 beta production by zymosan-stimulated monocytes with complement-activating hollow fiber as compared to noncomplement-activating hollow fiber before (1,411.9 +/- 865.7 +/- 149.9 pg/ ml/2 x 10(6) monocytes, p < 0.01). at the 15th minute (530.6 +/- 89.1 vs. 247.3 +/- 45.2 pg/ml/2 x 10(6) monocytes, p < 0.01) and at the end of dialysis (1,201.8 +/- 135.1 vs. 707.4 +/- 109.3 pg/ml/2 x 10(6) monocytes, p < 0.01). Similar results were observed with TNF-alpha production. IL-1 beta as well as TNF-alpha production decreased significantly at the 15th min of dialysis, thereafter they increased and approached the baseline levels towards the end of hemodialysis with both hollow fibers. Plasma C3a at the 15th minute correlated positively with postdialysis IL-1 beta and TNF-alpha production, while plasma C3a did not change in patients dialyzed with noncomplement-activating hollow fiber. Complement activation with complement-activating hollow fiber as well as monocyte-membrane interaction with complement-activating and noncomplement-activating hollow fiber might be involved in the pathogenesis of cytokine production during hemodialysis. Uremic toxin removal as well as stimulation of cytokine production inhibitor might contribute to the decreased cytokine production at the 15th minute of hemodialysis and monocyte-membrane interaction with or without complement activation resulted in augmented cytokine production toward the end of hemodialysis with both hollow fibers. We thus concluded that hollow fiber of bioincompatibility triggered much more cytokine production throughout the dialysis procedure.

Cellulose↗

PubMed1992

Complement activation during storage of blood under normal blood bank conditions. Effects of proteinase inhibitors and leukocyte depletion.

During storage of CPD-A1 preserved whole blood factors of the complement cascade become activated, as evidenced by a rapid increase in the concentrations of C3a-desArg and C4a-desArg. After 10 to 14 days of whole blood storage, the elevations of C3a and C4a levels were highly significant. This increase was paralleled by an increase in the concentration of the lysosomal proteinase elastase from polymorphonuclear (PMN) granulocytes. By contrast, the concentration of the C3 activator complex C4b2b remained unchanged even after 3 weeks of storage. The supplementation of the anticoagulant CPD-A1 with the polyvalent-proteinase-inhibitor aprotinin and the specific elastase-inhibitor eglin C failed to inhibit complement activation, whereas leukocyte depletion could partially abolish the increase of the concentration of C4a, but had no effect on C3a concentrations. These observations support the notion that cleavage of C4 during storage of whole blood is partially leukocyte dependent, whereas the activation of C3 is possibly caused by the activation of the alternate pathway of the complement system by contact of plasma with plastic surfaces.

Aprotinin↗

PubMedDate not supplied

The biology and pathophysiology of complement receptors.

Activation of the complement cascade leads to the generation of multiple breakdown products which bind on to specific cellular receptors and regulate their function. In this review, we describe the biochemical and physiological features of the 7 known complement receptors. Four of them (complement receptors 1, 2, and 3 and receptors for C3a) bind cleavage fragments of the third component of the complement and three have specificity for C1q, factor H and C5a. In patients with systemic lupus erythematosus, a unique human autoimmune disorder, the numbers of CR1 on the surface of the red blood cells are decreased; in this review we discuss the implications in the pathogenesis of SLE. A number of patients have now been reported whose cells lack CR3 from their surface; this deficiency is associated with a number of immune cell dysfunctions which are discussed in detail. Finally, we discuss aberrations in the expression of complement receptors in certain human leukemic cells.

Antigen-Antibody Complex↗

PubMed1983

Effects of particulate beta-1,3 glucan on human, rat, and guinea pig complement activity.

Particulate glucan, a beta-1,3-linked polyglucose derived from Saccharomyces cerevisiae, has been demonstrated to have a wide range of immunopotentiating effects. Glucan administration is associated with the modification of a variety of experimentally induced infectious disease states as well as the inhibition of growth of implantable and spontaneous tumors. The present study was designed to evaluate the effect of glucan upon activation of the complement system in rats and guinea pigs. Additional studies were performed to determine the in vitro activating effect of glucan and zymosan on complement activity of human serum. Glucan activated both the classical pathway of normal human sera and the alternate pathways in C2hu-deficient sera in vitro releasing anaphylatoxins such as C3a. The intravenous injection of glucan activated the alternate pathway of guinea pig plasma. The influence of glucan on complement depletion induced by cobra venom factor (CVF) was also ascertained. Complement activation by glucan may contribute, in part, to the enhanced resistance of the host against tumor growth as well as infectious episodes.

Animals↗

PubMed2000

Minor role of the C3a receptor in systemic anaphylaxis in the guinea pig.

Previously, Regal et al. [Regal, J.F., Fraser, D.G., Toth, C.A., 1993. Role of the complement system in antigen-induced bronchoconstriction and changes in blood pressure in the guinea pig. J. Pharmacol. Exp. Ther. 267, 979-988] demonstrated that preventing complement system activation resulted in inhibition of anaphylaxis in the guinea pig, and that the C-terminal 21 amino acids of guinea pig C3a (C3a-peptide) mimic the symptoms of anaphylactic shock in the guinea pig [Regal, J.F., 1997. Role of the complement system in pulmonary disorders. Immunopharmacology 38, 17-25]. To determine if C3a is an essential mediator of systemic anaphylaxis, the anaphylactic response to ovalbumin (OA) was assessed in guinea pigs genetically deficient in the C3a receptor (C3aR-) compared to their control strain of animals which were C3a receptor positive (C3aR+). In addition, the response to another control strain of animals, Hartley guinea pigs, was determined. Sensitized guinea pigs were anesthetized, and bronchoconstriction and changes in blood pressure were monitored in response to intravenous (i.v.) injection of either C3a-peptide, recombinant human C5a (rHuC5a) or OA. Both Hartley guinea pigs and C3aR+ animals responded similarly to C3a-peptide and rHuC5a. C3aR- animals, however, were unresponsive to C3a-peptide and responded normally to rHuC5a, confirming their functional deficiency of the C3a receptor. In response to OA, C3aR+ animals and Hartley guinea pigs responded with a severe bronchoconstriction, an initial transient hypotension, followed by an increase in blood pressure and a delayed prolonged hypotensive response. In contrast, in C3aR- animals, the increased blood pressure response to OA was significantly prolonged, the delayed hypotensive response was blunted, and the bronchoconstriction was delayed compared to the C3aR+ animals. The difference in the anaphylactic response could not be explained by differing amounts of OA-specific IgG1 antibody or C3a generated during the anaphylactic response. Thus, these data suggest that C3a plays a minor role in the hypotension of systemic anaphylaxis and investigation of a role for other products of complement system activation, either alone or in combination with C3a, is clearly warranted.

Anaphylaxis↗

PubMed1988

Limitation of complement activation by perfluorocarbon emulsions: superiority of lecithin-emulsified preparations.

A considerable body of evidence suggests that complement and granulocyte activation may be important in the occasional adverse reactions which occur on the administration of perfluorocarbon emulsions to patients. In an attempt to develop an emulsion which was less prone to activate complement than was the first product clinically tested, we devised an in-vitro protocol for the testing of an emulsion's ability to activate complement: emulsions were serially diluted, and were incubated with minimally-heparinized plasmas from each of several donors; the generation of C3a was assessed by commercial immunoassay. In such a system, F-Adamantane emulsions prepared with highly-purified lecithin as the emulsifier were consistently less complement-activating than comparable emulsions prepared with Pluronic F-68 as the emulsifier. Emulsification technique seemed unimportant, and HPLC fractionation of the Pluronics identified no innocuous subfraction. Application of these findings to an animal model is underway, to see if the superiority of lecithin-based emulsions is also evident in vivo.

Adamantane↗

PubMed1995

Monoclonal antibodies directed against human C5 and C8 block complement-mediated damage of xenogeneic cells and organs.

The hyperacute rejection (HAR) of xenotransplanted organs is initiated by the deposition of natural antibodies on donor endothelium followed by the activation of the recipient complement system, which rapidly destroys the graft. Studies of the role of activated complement in HAR have suggested that natural antibody as well as early (C3a, C3b) and late (C5a, C5b-9) activated complement components may contribute to cell activation and damage. Attenuation of HAR has been achieved by blockade of C3 activation with soluble CR1 or consumptive depletion of complement with cobra venom factor; however, similar studies using specific inhibitors of terminal complement components have not been described. To address the contribution of C5a and the membrane attack complex (C5b-9, MAC) to complement-mediated xenogeneic cell and organ damage, we utilized functionally blocking monoclonal antibodies directed against the human terminal complement components C5 and C8. Our data show that both anti-C5 and anti-C8 mAbs protect porcine aortic endothelial cells from membrane damage mediated by human C5b-9. Additionally, both the anti-C5 and anti-C8 mAbs blocked complement-mediated generation of membrane prothrombinase activity on porcine aortic endothelial cells challenged with human serum. To test the ability of these antibodies to attenuate antibody and complement-mediated damage of xenogeneic organs, an ex vivo model was developed wherein isolated rat hearts were perfused with human serum in the presence or absence of the anti-C5 and anti-C8 mAbs. Our data demonstrate that mAbs directed against human C5 and C8 prevented organ damage by human serum complement and suggest that these molecules may serve as potent inhibitors of HAR.

Animals↗

PubMed1983

Potentiation of the anaphylatoxins in vivo using an inhibitor of serum carboxypeptidase N (SCPN). I. Lethality and pathologic effects on pulmonary tissue.

Carboxypeptidase N (EC 3.4.12.7) (SCPN) is a plasma enzyme that efficiently inactivates the anaphylatoxins C3a and C4a and significantly reduces C5a spasmogenic activity by removing the C-terminal arginyl residue from each of these factors. The arginine analog DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid (SCPN-INH) is a potent competitive inhibitor of SCPN with a Ki for this carboxypeptidase in serum of 2 x 10(-9) M. Therefore, we have used the SCPN inhibitor to potentiate biologic activity of the anaphylatoxins in vivo. Infusion via the carotid artery of about 40 mg of SCPN-INH into each of 8 adult guinea pigs inactivated the SCPN for at least 3 hours and caused no measurable toxic effects. When cobra venom factor (CVF) is infused into guinea pigs, it activates the alternative pathway of complement, thereby generating the anaphylatoxins C3a and C5a. Ordinarily, infusion of CVF is nonlethal, because the generated anaphylatoxins are rapidly converted to C3a des Arg and C5a des Arg by SCPN. However, CVF (200 micrograms) plus SCPN-INH delivered intravenously in 5 animals induced a lethal reaction in less than 5 minutes. The authors conclude that the lethal effect is due largely to the anaphylatoxins. Histologic sections of the lungs from treated animals show dramatic structural changes consistent with peripheral small airway constriction, bronchial constriction, and vasoconstriction of small muscular arteries. Also, cell aggregates are present in blood vessels. Other histologic changes include severe congestion, pulmonary edema, and an interstitial infiltrate of mononuclear cells. Large doses of chlorpheniramine prevent this lethal reaction. Lethality is apparently attributable to asphyxia and is dependent on the level of CVF administered: eg, 100 micrograms CVF was not lethal in 4 animals given SCPN inhibitor, although signs of respiratory distress were observed. On histologic examination of lungs from guinea pigs given CVF and SCPN-INH, the features are similar to those described when anaphylatoxins are instilled into guinea pig lungs. Intravenous application of purified C3a plus SCPN-INH also proved lethal in 3 of the 6 animals challenged. This is the first evidence that the C3a anaphylatoxin can elicit a lethal response.

Anaphylatoxins↗