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PubMed2002

Immunoglobulin G subclass distribution of bullous pemphigoid autoantibodies and complement fixation studies.

OBJECTIVE: The purpose of this study was to examine the immunoglobulin G (IgG) subclass distribution of tissue bound and circulating antibasement membrane zone antibodies in bullous pemphigoid. In addition, the complement fixing capability of circulating IgG subclasses was also investigated. METHODS: Seventeen skin biopsies and 25 serum samples obtained from 25 cases of bullous pemphigoid were analyzed by direct and indirect immunofluorescence using mice anti-human IgG subclasses monoclonal antibodies. Indirect complement immunofluorescence was used to measure the avidity with which antibodies activate the complement. The study was carried out between 1992 and 1996 at the King Fahd Hospital of the University, Al Khobar, Kingdom of Saudi Arabia and the Western Infirmary Immunopathology Laboratory, Glasgow, Scotland. RESULTS: Immunoglobulin G1 deposits were detected in 10 of 17, IgG2 in one, IgG3 in 3 and IgG4 in 15 biopsies. Immunoglobulin G1 circulating antibodies were observed in 14, IgG2 in 0, IgG3 in 4 and IgG4 in 24 serum samples. Complement fixing antibodies were detected in 15 sera, 4 of which contained only IgG4 subclass. CONCLUSION: The predominance of IgG4 subclass observed in this study is similar to previously reported results. Complement fixation capability studies revealed non-complement fixing sera and the results were not compatible with the complement binding characteristics of IgG subclasses. This suggests that other mechanisms, which do not involve the complement, may participate in blister formation in bullous pemphigoid.

Autoantibodies↗
PubMed1998

Complement activation and inflammation triggered by model biomaterial surfaces.

Biomaterial-mediated complement activation repeatedly has been invoked as a trigger of phagocyte reactions and inflammation. However, a direct correlation between complement activation and inflammatory responses to biomaterial surfaces has yet to be established. Using an animal implantation model and gold surfaces bearing various thiol-linked functionalities, we investigated the potency of different surface groups in prompting complement activation in vitro and surface-mediated accumulation of inflammatory cells in vivo. Among the surfaces tested, mercaptoglycerol- and mercaptoethanol-bearing surfaces engendered the strongest inflammatory responses, as reflected by the accumulation of large numbers of adherent neutrophils and monocytes/macrophages. In contrast, L-cysteine-coated surfaces caused only minor inflammatory responses, and both glutathione-modified and untreated gold implants attracted minimal numbers of inflammatory cells. The accumulation of inflammatory cells on mercaptoglycerol surfaces appears to arise from surface-mediated complement activation because complement-depleted animals failed to exhibit inflammatory responses to mercaptoglycerol-modified implants. Furthermore, there is a close relationship between surface-mediated complement activation (as measured by in vitro iC3b/C5b-9 generation and C3 deposition) and in vivo inflammatory responses. At least in this animal model and with these model surfaces, our results indicate that surface-mediated complement activation can be responsible for the subsequent accumulation of inflammatory cells on implant surfaces.

Animals↗
PubMedDate not supplied

The genetics of the complement system.

It is suggested that the classical and alternative pathways of C3 activation and the terminal complement reaction pathway represent three replicates formed by gene duplication. It seems likely that the precursor system was what is now the alternative pathway and that its original function was a positive feedback loop for amplifying inflammatory reactions. These views are supported by physicochemical data on the complement components; by genetic data; and by similarities in the reaction patterns. Study of subjects with isolated complement component deficiencies provides information on the function of complement in vivo. It has been found that complement component deficiency is associated with bacterial infection, particularly with Neisseria; and even more so with immune complex disease. This second, rather surprising, association is likely to be the result of a requirement for complement in the catabolism of immune complexes on the one hand, and the need for an intact complement system to eliminate low virulence infectious organisms on the other.

Biological Evolution↗
PubMedDate not supplied

Intraarticular activation of the complement system in patients with juvenile rheumatoid arthritis.

Analyses of CH50, complement components, properdin factors, and kininogen in synovial fluid of patients with juvenile rheumatoid arthritis revealed evidence of activation of the classic complement pathway in all clinical subgroups. Juveniles with the adult pattern of disease had the greatest incidence of complement abnormalities. Evaluation of individual components by both activity determination and protein measurement showed decreased synovial fluid specific functional activity (activity per microgram protein) to the more marked in synovial fluids with profound depressions of complement activity. These findings provide further evidence that nonfunctional, antigenically intact component protein may remain after complement activation. Radial immunodiffusion measurements of properdin factors and kininogen failed to support their involvement in joint inflammation. Serum complement component measurements by activity but not protein concentration correlated with other parameters or inflammation. Four patients had isolated depressions of serum C2 activity. Immunoglobulin levels, particularly IgA, correlated with some complement measurements and with the sedimentation rate.

Adolescent↗
PubMed1979

Antibody-independent activation of complement by human peripheral B lymphocytes.

Normal human peripheral blood lymphocytes were shown to activate complement in normal human serum (NHS). This activation led to C3 fixation on the cell membrane, which in turn was visualized by fluorescence. The reaction occurred in the absence of detectable amounts of antibodies, since an agammaglobulinemic patient's serum also supported complement activation, and the results were unaltered by absorption of normal human serum. Trypsin treatment of lymphocytes to remove possible complement activators bound to the cell membrane, did not have any effect on the complement activation by lymphocytes. Complement membrane fluorescence was abolished in the presence of EDTA or ethyleneglycolbis(aminoethylether) tetraacetate (EGTA) supplemented by Mg++ions indicating that the classical pathway of complement activation was involved in the reaction. Experiments performed with T and B-purified populations showed that the phenomenon was confined to the B cell fraction. Complement deposition did not diminish the number of EAC rosettes, and viability remained unchanged after exposure of lymphocytes to normal human serum.

Agammaglobulinemia↗
PubMed1994

Targeted neutralization of the complement membrane attack complex inhibitor CD59 on the surface of human melanoma cells.

Major problems in the immunotherapy of human tumors with complement-activating monoclonal antibodies (mAb) are (i) inherent resistance of tumor cells to complement cytolysis and (ii) a possible undiscriminatory attack against normal cells. In the present study we have developed a procedure to simultaneously direct the complement membrane attack complex and neutralize its inhibitor CD59 (protectin) on human melanoma cells in vitro. G361 melanoma cells were selectively recognized in heterogenous cell mixtures by a complement-fixing mAb (R24) against the tumor cell GD3-ganglioside. Biotinylated anti-CD59 mAb (YTH53.1) was directed to the tumor cells with a high-affinity biotin-avidin bridge using a proportion of R24 as a biotinylated targeting mAb and avidin as a linker. Biotinylated anti-CD59 mAb lost its ability to activate complement, but retained its CD59-neutralizing activity. Thus, it was possible to avoid nonspecific lysis of surrounding erythrocytes and endothelial cells and direct the CD59-neutralizing effect to the tumor cells. As a result the tumor cells were efficiently killed by R24 plus complement while the bystander cells remained viable. These results suggest that it is possible to target an unrestricted complement membrane attack against GD3- and CD59-positive melanoma cells.

Antibodies, Monoclonal↗
PubMed2005

Flavonoids from the leaves of Litsea japonica and their anti-complement activity.

Four flavonoids, epicatechin (1), afzelin (2), quercitrin (3), and tiliroside (4), were isolated from the leaves of Litsea japonica (Thunb.) Jussieu (Lauraceae). The structures of compounds were identified by comparing their chemical and spectral data with those previously reported. The flavonoids (1-4) were tested for their anti-complement activity against classical pathway of complement system. Compounds 2-4 showed inhibitory activity against complement system with IC50 values of 258, 440, and 101 microm, respectively, whereas 1 was inactive. For the evaluation of the structure-activity relationship of 5,7-dihydroxyflavones, myricitrin (5) from Juglans mandshurica also tested for it's anti-complement activity and is inactive in this assay system. Furthermore, compounds 2, 3, and 5 were hydrolyzed with naringinase to give kaempferol (2a), quercetin (3a), and myricetin (5a), and these were also tested for their activity. Of the three aglycones, 2a exhibited anti-complement activity with an IC50 value of 730 microM, while 3a and 5a were inactive. The inhibitory potencies of 2, 2a, 3, 3a, 5, and 5a against complement activity increased in inverse proportion to number of free hydroxyls on B-ring of 5,7-dihydroxyflavone. Of the compounds tested, 4 showed the most potent inhibitory activity against the complement system.

Complement Inactivator Proteins↗
PubMed1994

Selective, prolonged alteration of complement-mediated immune clearance after acute exposure of mice to ethanol.

A selective and prolonged alteration in complement-mediated immune clearance was found in mice given a single intraperitoneal injection of ethanol. Rate constants for the separate components of complement- and IgG Fc gamma-mediated clearance were determined using a branched series, first-order reaction sequence model and measurements of the disappearance of radiolabeled IgG-opsonized murine erythrocytes from the circulation of BALB/c mice. The rate constant governing immune clearance mediated by IgG Fc gamma receptors (k3) decreased to 16% of control at 1 hr after ethanol injection but returned to normal in 72 hr. A > 50% decrease in complement-mediated clearance occurred, with a nadir of complement-mediated sequestration (k1) and complement-dependent phagocytosis (k4) at 1 hr (P < 0.001). In this case, however, k1 and k4 rate constant values did not return to control levels until 6 weeks after the injection of ethanol. The rate constant governing C3b deactivation and release of deactivated, sensitized cells back to the circulation before they undergo phagocytosis (k2) was initially normal, but decreased in Week 6 and remained low to the end of the observation period at 22 weeks (P < 0.0001). These changes resulted in a major reduction in overall complement-mediated immune clearance up to 4 weeks after the ethanol injection. The change to normal rates for sequestration and phagocytosis coupled with decreased deactivation and release at 6 weeks postinjection resulted in a small increase in overall complement-mediated clearance that persisted through Week 22.

Alcohol Dehydrogenase↗
PubMed1994

Endothelium-dependent microvascular responses to activated complement.

Infusion of Escherichia coli bacteria to cause high cardiac output bacteremia produces a differential microvascular response with constriction of large arterioles and dilation of small arterioles in skeletal muscle of rats. An important component to host-defense mechanisms during bacteremia is activation of the complement system. One part of this study explored the possibility that microvascular responses to bacteremia could be mediated by activation of the alternative complement cascade to alter skeletal muscle blood flow during sepsis. Complement activation by iv zymosan into unanesthetized (decerebrate) Sprague-Dawley rats caused constriction of large arterioles and dilation of small arterioles in cremaster muscle, while cardiac output stayed normal or was elevated. These microvascular responses mimic those during bacteremia, suggesting that components of the complement system mediate skeletal muscle microcirculatory responses to live E. coli sepsis. The vasodilation response of small arterioles in skeletal muscle during bacteremia is endothelium-dependent and is mediated at least partially by endothelial-derived relaxing factor (EDRF). Complement activation gives products which interact with endothelial cells. Thus, a second part of this study explored the role of EDRF in the vasodilation of skeletal muscle small arterioles during activation of the alternate complement pathway. Blockade of EDRF action by hydroquinone totally abolished small arteriole dilation and large arteriole constriction responses to complement activation by zymosan infusion.

Animals↗
PubMed1992

The role of complement-derived mediators in inflammatory skin diseases.

The complement system represents an important nonspecific skin defense mechanism. Its activation leads to the generation of products that not only help to maintain normal host defenses but also mediate inflammation and tissue injury. Proinflammatory products of complement include large fragments of C3 with opsonic and cell-stimulatory activities (C3b and C3bi), low molecular weight anaphylatoxins (C3a, C4a, and C5a), and membrane attack complex. Among them C5a or its degradation product C5a des Arg seems to be the most important mediator because it exerts a potent chemotactic effect on inflammatory cells. Intradermal administration of C5a anaphylatoxin induces skin changes quite similar to those observed in cutaneous hypersensitivity vasculitis that occurs through immune complex-mediated complement activation. Complement activation is involved in the pathogenesis of the inflammatory changes in autoimmune bullous dermatoses. In pemphigus complement activation by pemphigus antibody in the epidermis seems to be responsible for the development of characteristic inflammatory changes termed eosinophilic spongiosis. In bullous pemphigoid (BP) interaction of basement membrane zone antigen and BP antibody leads to complement activation that seems to be related to leukocytes lining the dermoepidermal junction. Resultant anaphylatoxins not only activate the infiltrating leukocytes but also induce mast cell degranulation which facilitates dermoepidermal separation and eosinophil infiltration. Similar complement activation seems to play a more direct role in the dermoepidermal separation noted in epidermolysis bullosa acquisita and herpes gestationis. Anaphylatoxin generation via the alternative pathway activation under light irradiation is implicated in the development of the immediate erythematous phototoxic reactions induced by such well-known chemicals as porphyrin, chlorothiazide, demethylchlortetracycline, and chlorpromazine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acne Vulgaris↗
PubMed1993

Complement in human reproduction: activation and control.

The behaviour of the complement system during human reproduction is now the focus of much scientific attention. The presence of antisperm antibodies in the reproductive tracts of some infertile individuals, and of complement in cervical and ovarian follicular fluid, suggests that complement-mediated damage of spermatozoa is involved in some cases of infertility. Further, deposition of maternal IgG and of complement in the extrafetal tissues indicates that complement activation occurs within the fetoplacental unit. Recently, three complement-regulatory proteins--decay-accelerating factor, membrane cofactor protein and CD59--have been detected on spermatozoa and in the extrafetal tissues. It is likely that these inhibitors are essential for normal reproductive function. This article reviews current understanding of the interaction of the complement system with cells and tissues involved in reproduction, with emphasis on the nature and function of the controlling proteins.

Complement Activation↗
PubMed1986

Schistosoma mansoni: killing of transformed schistosomula by the alternative pathway of human complement.

The interaction of mechanically transformed schistosomula of Schistosoma mansoni with the alternative pathway of human complement was studied in vitro. To detect early changes in transformation, the schistosomula were prepared at a low temperature and used immediately. As shown previously, freshly transformed schistosomula were highly susceptible to killing by normal human serum and by C4-depleted normal human serum. This serum activity was concentration dependent and was markedly reduced on a twofold serum dilution. Upon incubation at 37 C in defined synthetic medium, schistosomula rapidly became refractory to killing by the alternative pathway of complement. After 1 hr of incubation at 37 C, the percentage of schistosomula which were resistant to killing increased from 16 to 85. This conversion was accompanied by a fivefold decrease in deposition of C3b on schistosomula which had been exposed to 37 C for 1 hr and then further incubated with C4-depleted normal human serum. The following events occurred concomitantly during incubation of freshly transformed schistosomula at 37 C with a half-life of 30-60 min: (1) Decrease in activation and consumption of the alternative pathway of complement by schistosomula; (2) appearance of a strong complement consuming activity in the supernatant of incubating schistosomula; and (3) shedding of protein- and carbohydrate-containing substances from the surface of schistosomula into the supernatant. Isolated external membranes of freshly transformed schistosomula consumed the alternative pathway of complement to a greater extent than membranes of schistosomula preincubated in medium at 37 C. The results demonstrate that transformed schistosomula acquire resistance to complement killing via the alternative pathway by shedding complement-activating substances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Lytic rabbit IgG for tissue culture trypomastigotes of Trypanosoma cruzi alters the extent and form of complement deposition.

Infective and vertebrate stages of Trypanosoma cruzi are resistant to lysis by the alternative pathway of complement. To further elucidate the mechanism of complement evasion and to study how some immune sera render the infective stage sensitive to lysis, we compared the interaction of complement components C3 and C9 with the surface of complement susceptible, vector stage epimastigotes and vertebrate stage trypomastigotes of T. cruzi. Our studies showed that, upon incubation in human serum, complement resistant tissue culture trypomastigotes (TCT) bound five- to eightfold less C3 or C9 than complement sensitive epimastigotes (Epi). C3 bound to Epi is mainly in the hemolytically active C3b form, while TCT bear predominantly the hemolytically inactive iC3b fragment, which cannot participate in C5 convertase formation or lead to deposition of the lytic C5b-9 complex. Three- to sixfold more C3 and two- to threefold more C9 were deposited on TCT when lytic rabbit immune IgG with broad specificity was used to sensitize the parasites, and nearly one-half of bound C3 was present as C3b. In contrast, a comparison of three different sources of IgG from immune human serum showed a less clear correlation between the titer or specificity of anti-T. cruzi antibody, enhancement of C3 or C9 deposition, change in the form of bound C3, or killing. These results show that lytic rabbit IgG for T. cruzi changes the form and amount of bound complement components in anticipated fashion, but that human immune IgG does not give predictable changes in the extent or form of C3 or C9 deposition.

Animals↗
PubMed1983

Precipitability and composition of HBsAg-anti-HBs immune complexes formed in the presence of complement. A model of circulating immune complex analysis.

Immune complexes (IC) of partially purified HBsAg and human anti-HBs were prepared at different antigen/antibody ratios in the presence of complement in normal human serum (NHS), and under conditions not allowing complement activation in buffers or in NHS containing 10 mM EDTA (NHS-EDTA). Commercial preparations of the radiolabelled antigen and antibody were used. IC formed in NHS were not significantly precipitated even after incubation for 24 h at 4 degrees C, whereas a typical precipitation curve was observed with complexes formed in the absence of complement. Thus, complement activation was found to markedly and permanently inhibit precipitability of HBsAg-anti-HBs immune complexes (HBsAg-IC). HBsAg-IC were precipitated from sera with 3.5% polyethylene glycol (PEG), boiled in sodium dodecyl sulphate (SDS)-urea buffer, and analysed by SDS-polyacrylamide slab gel electrophoresis (SDS-PAGE). With complexes formed in the presence of complement, about one-sixth of the antibody activity was found in high molecular weight fractions corresponding in size to IgG oligomers. By contrast, with complexes formed without complement, no significant amount of antibody was found in these fractions. With blotting technique and radiolabelled anti-human-C3 antibody, it was demonstrated that anti-HBs was covalently bound to C3b fragments in IC formed in the presence of complement and was in the high molecular weight fractions.

Animals↗
PubMed1986

Modulation of serum complement levels following exposure to polychlorinated dibenzo-p-dioxins.

Subchronic 14-day exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed serum total hemolytic complement activity (CH50) in female B6C3F1 mice at doses of 0.01, 0.05, 0.1, 0.5, 1.0, and 2.0 micrograms/kg. Serum levels of complement component C3 were also suppressed at doses of 0.5, 1.0, and 2.0 micrograms/kg. Another dioxin isomer, 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (HCDD), also produced dose-dependent suppression of complement activity at doses of 0.1, 1.0, and 10 micrograms/kg with decreased C3 levels at 10 micrograms/kg. Both TCDD and HCDD enhanced susceptibility to Streptococcus pneumoniae, a bacterial pathogen whose host defense is complement mediated. Recovery studies demonstrated that complement activity in TCDD (1 microgram/kg) and HCDD (10 micrograms/kg)-treated animals was suppressed until 50 days post-treatment, while low doses of HCDD (0.1 and 1.0 micrograms/kg) elevated CH50 levels. Acute exposure to TCDD (14 micrograms/kg) also suppressed complement CH50 and C3 levels. These studies demonstrate that the complement system and innate immunity represent potential target sites for polychlorinated dibenzo-p-dioxins.

Administration, Oral↗
PubMed1990

Significance of urinary complement components in various glomerular diseases.

The concentrations of two components of the complement system (C1q and C3) were measured in the urine and blood in 10 normal subjects and 134 patients with primary and secondary glomerulonephritis by using a highly sensitive enzyme immunoassay. The values of urinary excretion of C1q and C3 were well correlated to the ratios of fractional clearance of these complement proteins to that of neutral dextran of 55 A, which was used to minimize the influences of glomerular sieving because of their comparable molecular size to these complement components. The rate of renal tubular reabsorption of C1q and C3 were at least 89.2 and 93.4% of filtrated C1q and C3, respectively. Urinary C1q and C3 were excreted significantly in cases of membranoproliferative glomerulonephritis (MPGN), membranous glomerulonephritis, IgA nephropathy with both mesangial and capillary immune complex (IC) deposit and also in case of active lupus nephritis. On the other hand, the concentrations of these complement components were low in case of minimal lesion nephrotic syndrome, mild proliferative glomerulonephritis, inactive lupus nephritis and diabetic nephropathy without any immune staining. There was a significant correlation between the urinary excretion of C1q or C3 and intraglomerular IC deposition, especially IC deposition along the glomerular capillary wall. However, the degree of the excretion of these proteins was not correlated to the degree or permselectivity of proteinuria. The correlations between urinary C1q and C3 were observed in cases of IgA nephropathy with both mesangial and capillary deposit and MPGN, although we couldn't see the correlation in the other glomerular diseases. It is suggested that urinary excretion of such complement components represents the fixation of complement by deposited intraglomerular IC. The measurement of urinary concentration of these complement components provides a new clue to investigation or diagnosis of glomerular diseases.

Arginine↗
PubMed1995

In vitro and in vivo inhibition of complement activity by a single-chain Fv fragment recognizing human C5.

Complement activation has been implicated in the pathogenesis of several human diseases. Recently, a monoclonal antibody, (N19-8) that recognizes the human complement protein C5 has been shown to effectively block the cleavage of C5 into C5a and C5b, thereby blocking terminal complement activation. In this study, a recombinant N19-8 scFv antibody fragment was constructed from the N19-8 variable regions, and produced in both mammalian and bacterial cells. The N19-8 scFv bound human C5 and was as potent as the N19-8 monoclonal antibody at inhibiting human C5b-9-mediated hemolysis of chicken erythrocytes. In contrast, the N19-8 scFv only partially retained the ability of the N19-8 monoclonal antibody to inhibit C5a generation. To investigate the ability of the N19-8 scFv to inhibit complement-mediated tissue damage, complement-dependent myocardial injury was induced in isolated mouse hearts by perfusion with Krebs-Henseleit buffer containing 6% human plasma. The perfused hearts sustained extensive deposition of human C3 and C5b-9, resulting in increased coronary artery perfusion pressure, end-diastolic pressure, and a decrease in heart rate until the hearts ceased beating approximately 10 min after addition of plasma. Hearts treated with human plasma supplemented with either the N19-8 monoclonal antibody or the N19-8 scFv did not show any detectable changes in cardiac performance for at least 1 hr following the addition of plasma. Hearts treated with human plasma alone showed extensive deposition of C3 and C5b-9, while hearts treated with human plasma containing N19-8 scFv showed extensive deposition of C3, but no detectable deposition of C5b-9. Administration of a 100 mg bolus dose of N19-8 scFv to rhesus monkeys inhibited the serum hemolytic activity by at least 50% for up to 2 hr. Pharmacokinetic analysis of N19-8 scFv serum levels suggested a two-compartment model with a T1/2 alpha of 27 min. Together, these data suggest the recombinant N19-8 scFv is a potent inhibitor of the terminal complement cascade and may have potential in vivo applications where short duration inhibition of terminal complement activity is desirable.

Amino Acid Sequence↗
PubMed1996

In vivo effects of various therapies on complement-sensitive erythrocytes in paroxysmal nocturnal hemoglobinuria.

The percentage of complement-sensitive erythrocytes varies among patients with paroxysmal nocturnal hemoglobinuria (PNH) and is related to disease severity. We examined the changes of complement-sensitive erythrocytes following administration of androgens, prednisolone, dextran, and iron to 12 PNH patients using the complement lysis sensitivity test or flow cytometric analysis of decay accelerating factor and CD59/membrane attack complex-inhibitory factor expression for 11 years. Five untreated PNH patients were also studied as a control group. The complement-sensitive erythrocyte count remained almost constant in the control group, while it increased in four out of five patients receiving androgens. In addition, it decreased in two out of three patients receiving prednisolone, increased in both patients treated with dextran, and increased slightly in two of the three patients receiving iron therapy. Episodes of hemoglobinuria increased in three of the nine patients showing an increase of complement-sensitive erythrocytes, and decreased in four patients receiving prednisolone or dextran. A good response to treatment was clinically observed in four patients receiving androgens, in one patient treated with prednisolone, and in one patient receiving dextran according to the scoring system. These findings suggest that PNH remains stable when the number of complement-sensitive erythrocytes remains fairly constant, and that the PNH III erythrocyte count is especially related to the frequency of hemoglobinuria. Thus, it seems to be important to determine the long-term effect of drug therapy on complement-sensitive erythrocytes to select the most appropriate treatment.

Adolescent↗

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