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PubMed1992

Complement activation in neonatal infection.

To investigate the usefulness of indices of complement activation in the diagnosis of infections in the neonatal period, activation products C4d, Ba, and C3d were measured in 42 babies with a putative diagnosis of infection based on clinical/laboratory criteria, and compared with conventional clinical and haematological criteria of infection and with C reactive protein. The diagnosis of sepsis was confirmed by culture and identification of organisms in 17. Fourteen babies in whom infection was not suspected formed the control group. In babies with proved infection, concentrations of the fragments C4d, Ba, and C3d were higher than in babies with suspected infection in whom microbiological tests were negative, and concentrations of Ba and C3d were higher than in controls. C reactive protein and the platelet count were not significantly different in babies with proved infection and those with negative microbiological tests, but in the latter, C reactive protein concentrations were higher than in controls. Of the indices studied, high concentrations of Ba predicted microbiologically proved infection with the highest sensitivity (47.1%) and specificity (92.0%). Ba thus seems to be useful as an early indicator of infection in the neonatal period.

Analysis of Variance↗

PubMed1992

Immunological studies in placentas with villitis of unknown etiology: complement components and immunoglobulins in chorionic villi.

Villitis of unknown etiology (VUE) is a common placental lesion and complement-fixing immune complexes is one of the mechanisms proposed for its development. We examined 16 placentas with VUE and 16 without VUE by immunofluorescence in order to compare the distribution and amount of C1q, C3d, IgG and IgM in the chorionic villi between the two groups. We found both in cases with and without VUE a distribution of the complement components and immunoglobulins similar to that described in normal placentas. The amount of deposit was also not significantly different in the two groups. Only the inflamed villi showed an abnormal distribution of C1q which was present diffusely in the stroma of these villi.

Chorionic Villi↗

PubMed1987

Activation of fibrinolysis during xenoperfusion.

Ten rabbit kidneys were perfused at 80 mm Hg, 37 degrees C, with oxygenated recirculating heparinized human blood. These experiments were compared to another ten perfusion experiments where 1 unit/ml porcine plasmin was added to the human blood one hour before the perfusion, at which time the fibrinolytic activity was significant and the fibrinogen concentration under the detection limit. Rejection, determined as time until blood flow decreased to 2 ml/min, was not significantly delayed by addition of plasmin. At the end of the experiments, the fibrinolytic activity in the control experiment had increased above the activity in the plasmin added experiments, although the fibrinogen concentration was almost unchanged. Histological examinations demonstrated a decreased platelet deposition and the fall in platelet count was smaller in the plasmin experiments. C3d determinations revealed a slight activation of complement upon addition of plasmin, but the activation by xenoperfusion was much more pronounced and, at the end of the experiment, the C3d concentration was the same in the two groups.

Animals↗

PubMed1983

High levels of complement breakdown products in tuberculous pleural effusions.

Pleural fluids from 10 patients with tuberculous pleural effusions contained high levels of small molecular weight breakdown products of C3 (C3d) and of properdin factor B (Ba) when compared to 16 patients with effusions of neoplastic origin (P less than 0.001). The same fluids exhibited overlapping values of haemolytic factor B, classical or alternative pathway-mediated haemolytic activity and native C3. A significant correlation between Ba and lysozyme levels was found in all effusions tested (P less than 0.05). These findings suggest that activation of the complement system is an important aspect of the extensive inflammation and tissue destruction characteristic of human tuberculosis.

Complement Activation↗

PubMed1985

Complement levels and C3 breakdown products in open-heart surgery: association of C3 conversion with the postpericardiotomy syndrome.

The role of the complement system in the pathogenesis of the post-pericardiotomy syndrome (PPS) was evaluated in a prospective study by measuring the levels of complement (C) components, total haemolytic complement activity and circulating C3 breakdown products in serial plasma and serum samples of 45 patients undergoing open-heart surgery. A consistent reduction in the levels of C3 and C4 but not of factor B was seen on the second post-operative day. During the second post-operative week the antigenic levels of each C component increased significantly. At this time six patients developed the post-pericardiotomy syndrome. Circulating C3 conversion products (C3bi and C3c) were demonstrated in the plasma samples from five of these patients by the immunofixation technique, the mean conversion percentage being 14.3 +/- 10.6. The samples from 15 of the 39 other patients also showed C3 conversion, but the mean percentage was significantly lower (4.5 +/- 6.1%, P less than 0.05). Before the second post-operative week C3 conversion was rare in both groups. The C3d levels of plasma samples, as detected by rocket immunoelectrophoresis, followed a similar pattern. Reduced total haemolytic complement activity was found in three patients suffering from the PPS. These results suggest a role for complement in the non-infectious, inflammatory response during the late post-operative period after open heart surgery, and especially in the post-pericardiotomy syndrome.

Adolescent↗

PubMed1992

T lymphocyte expression of complement receptor 2 (CR2/CD21): a role in adhesive cell-cell interactions and dysregulation in a patient with systemic lupus erythematosus (SLE).

Complement receptor 2 (CR2, CD21), the receptor for both the C3d,g portion of human complement component C3 and the Epstein-Barr virus, has been recently described on peripheral T cells. By using dual stain flow cytometric analysis, we have also observed that a peripheral T lymphocyte subpopulation of normal healthy donors bears CR2 in a range varying from 1.1 to 23.2% (mean 12.6%) of total CD3+ cells. T lymphocytes from nine patients with inactive SLE expressed CR2 in a similar range. Three patients with active SLE were also studied. One of them, having neuropathy and glomerulonephritis, displayed an expansion of the CR2 T cell subpopulation which reached as much as 89% of total CD3+ cells. To examine potential functional roles of T cell CR2, cells from a Jurkat-derived CR2 expressing T cell line were found to bind in vitro to human CR2-, complement-coated K562 cell targets in a CR2- and complement-dependent fashion. Based on these studies, we hypothesize that CR2 might act to increase adherence of T cells to nucleated target cells bearing C3d,g, a function which may be relevant to cytotoxicity or other T cell activities requiring cell-cell interaction.

B-Lymphocytes↗

PubMed1988

Complement C3 and C5 degradation products during hemodialysis treatment: study of an index of membrane bioincompatibility.

In 10 hemodialyses (HD) with cuprophan (CU) and 10 with polyacrylonitrile (PAN), signs of complement activation were investigated by following arterial and venous levels of C3a, C3d and C5a, in order to propose a marker of bioincompatibility. Despite large individual variabilities, significant increases of these molecules were detected at t 20 min, particularly with CU device in the artery and more marked in the vein except for C3d with PAN. During the later stage of HD, while C3a and C5a levels gradually declined, but remained significantly higher than t 0 in all the patients treated with CU, the C3d concentration reached a plateau suggesting a continuous complement activation throughout HD. HD using PAN membranes were associated with a lower C3a, C3d and C5a generation and fewer dialyses generating these products. In some dialyses the higher arterial level of these molecules suggests an extra-dialyzer complement activation especially with PAN membrane. Although C5a venous levels appeared to be the more significant index of complement activation, for clinical purposes we propose the C3d arterial measurement as a reliable, non-expensive and technically simple indicator of membrane intolerance.

Acrylic Resins↗

PubMed1992

Plasma concentrations of fibronectin and C3d in patients with amoebic liver abscess.

By means of simple and specific ELISA techniques, the plasma concentrations of soluble fibronectin and C3d, a breakdown product of C3 complement, were determined in patients with amoebic liver abscesses (ALA) and in healthy controls. The mean plasma fibronectin concentrations in 23 patients with ALA and in 20 controls were found to be 441 +/- 89 mg/l and 442 +/- 66 mg/l, respectively. The difference between these two values was not statistically significant. The mean C3d value in 21 patients with ALA, however, was found to be 84 +/- 14 AU/l which was significantly different from the value of 12 +/- 4.7 AU/l noted in 20 healthy persons. Plasma concentrations of these two proteins are discussed in relation to their possible implications in the immunopathogenesis of amoebic liver abscess.

Complement C3d↗

PubMed1989

Persistent complement activation in submucosal blood vessels of active inflammatory bowel disease: immunohistochemical evidence.

Extensively washed and ethanol-fixed colonic specimens from 10 patients with ulcerative colitis, 3 patients with Crohn's disease of the colon, and 8 histologically normal controls were examined by two-color immunohistochemistry with monoclonal antibody to a neoepitope in the terminal complement complex combined with antiserum to factor VIII-related antigen (von Willebrand's factor), C3c, C3d, or C5. An alternative combination was monoclonal antibody to S-protein and antiserum to C9. Submucosal vessel walls in both normal and diseased colon showed parallel positivity for C3d, C5, C9, terminal complement complex, and S-protein, but the staining intensity and the proportion of positive vessels were significantly higher in inflammatory bowel disease than in controls. In addition, there was significantly more C3c reactivity associated with the terminal complement complex-positive submucosal vessels of active inflammatory bowel disease lesions than in histologically normal colon. Vascular C activation may therefore be a continuous process in active inflammatory bowel disease lesions, presumably related to the degree of inflammation and immune complex formation.

Adolescent↗

PubMed1988

Complement receptors CR1 on human peripheral nerve fibres.

Receptors for C3 and C4 in human peripheral nerve tissue were studied by examining the adherence of complement (C) coated erythrocytes (E) and by using monoclonal antibodies against epitopes on the receptors for C3b (CR1), C3d (CR2) and C3bi (CR3). E (erythrocyte)-bearing C3b or C4b adhered to sections of myelinated peripheral nerves and the binding was inhibited only by anti-CR1 antibodies. By immunofluorescence, anti-CR1 antibodies stained the nerve fibres, whereas anti-CR2 and anti-CR3 antibodies did not. The staining was apparently localized to the Schwann cell membrane. E-bearing C3bi or C3d did not adhere to myelinated or unmyelinated nerves. CR1 are therefore the only C3 receptors expressed in human peripheral nerves. E-bearing C3b or C4b did not adhere to unmyelinated nerves from adults or to nerves from fetuses at a gestational age of approximately 21 weeks, whereas monoclonal anti-CR1 antibodies stained myelinated, unmyelinated and fetal nerves equally well. The results indicate that CR1 in unmyelinated and fetal nerves are either functionally inactive or express a lower affinity for C3b/C4b than CR1 in myelinated nerves. There were no significant differences in the binding of E-bearing C3b or C4b to myelinated peripheral nerves from 50 individuals, indicating that CR1 activity is not distributed phenotypically.

Adult↗

PubMed1982

Correlation in rheumatoid arthritis of concentrations of plasma C3d, serum rheumatoid factor, immune complexes and C-reactive protein with each other and with clinical features of disease activity.

The concentrations of C3d in the plasma and of C-reactive protein (CRP), immune complexes and rheumatoid factor in the serum were measured in 99 patients with rheumatoid arthritis. Most patients had raised levels, the values of which correlated with disease activity assessed according to a newly described index based on multivariate analysis of subjective, semi-objective and objective features of the disease. There were also significant correlations between the values for plasma C3d and circulating immune complexes, immune complexes and rheumatoid factor, serum CRP and immune complexes, and serum CRP and plasma C3d. Measurement of plasma C3d provides a useful means of detecting in vivo complement activation, which may be involved in the pathogenesis of rheumatoid arthritis, but neither C3d levels nor any of the other variables correlated as closely with disease activity as did the serum CRP concentration.

Adult↗

PubMed1986

Complement C3b receptors on erythrocytes, circulating immune complexes, and complement C3 split products in patients with primary Sjögren's syndrome.

Twenty-one patients with primary Sjögren's syndrome (SS) and 22 age- and sex-matched healthy controls were examined for levels of C3b receptors (CR1) on erythrocytes (by an enzyme-linked immunosorbent assay), levels of circulating immune complexes (IC) (by a polyethylene glycol precipitation complement consumption method), and C3 split products, C3d and C3c (by intermediate gel rocket immunoelectrophoresis). CR1 varied within a wide range (20-124%), and a preponderance of low numbers was found among patients with primary SS (P less than 0.05). The levels of circulating IC and C3d were elevated in primary SS patients (P less than 0.01) and were mutually correlated (P less than 0.01; tau = 0.5), but levels of circulating IC and C3d did not correlate with CR1 values. C3c concentrations were the same in patients and controls. It is possible that the CR1 level serves as a predictor for the development of IC-induced manifestations, and the C3d concentration serves as an objective parameter for disease activity in primary SS.

Adult↗

PubMed1995

A functional role for corpora amylacea based on evidence from complement studies.

Few theories have been advanced for the production of corpora amylacea (CA) by the normal ageing brain and by the CNS under various neurological conditions. Proteins derived from neurons and oligodendrocytes are found in CA and to understand their origins brain tissue from patients with Alzheimer's disease (AD), multiple sclerosis (MS) and Pick's disease (PD) were tested for complement activity. All CA were immunopositive for antisera to classical pathway-specific components, the activation products C3d and the terminal complement complex (TCC), the C3 convertase regulator membrane cofactor protein (MCP) and the fluid phase regulators S-protein and clusterin. CA were immunonegative for the alternative complement pathway proteins and the complement regulators, decay accelerating factor (DAF) and CD59. Western immunoblotting of isolated solubilized CA from the same tissues demonstrated a weak band for MCP but TCC was more easily shown by immunoprecipitation. A filamentous fringe around CA, probably of astrocytic origin, was also immunopositive for complement factors. CA consist of an inert mucopolysaccharide matrix encasing ubiquitinated proteins, resulting from death of and damage to neurons, myelin and oligodendrocytes. A function of CA, therefore, could be to prevent the recognition of these immunogenic proteins by lymphocytes and microglia and thus protect the CNS from further injury.

Aging↗

PubMed1977

Comparison of low-molecular-weight products following reaction of C3-C3b with C3b inactivator and with trypsin.

Substitution of trypsin for Konglutinogen-activating factor (KAF) in the procedure for cleaving C3d from C3-C3b substrate produced a relatively heterogeneous low-molecular-weight fraction (C3d-Tryp) which differed in a number of ways from the KAF-mediated cleavage product (C3d-KAF). The differences were demonstrable by agar and polyacrylamide gel electrophoresis, 125I-labelling, content of immunoreactive 125I-labelled C3d, inhibition of anti-complement antiglobulin reagents and rabbit immunization. By comparison with C3d-KAF, the C3d in C3d-Tryp was more heterogeneous and exhibited a faster electrophoretic mobility in agar at pH 8.6. By contrast to C3d-KAF, C3d-Tryp contained protein carrying C3c antigenic determinants.

Complement C3↗

PubMed2003

Was it there all the time?

The complement system is old, yet it may still have something new to teach us. For many years, research has existed which shows that C3d, in addition to its established role as an adjuvant, could have an immunosuppressive activity. Being true, it suggests that a common mechanism may be used both by organisms and by their pathogens to prevent unwanted immune responses.

Animals↗

PubMed1983

Studies of the Epstein Barr virus receptor found on Raji cells. II. A comparison of lymphocyte binding sites for Epstein Barr virus and C3d.

A comparison was made between the binding sites of two receptors that are believed to be closely associated on human B lymphocytes: complement receptor type two (CR2) that is specific for C3d fragments, and the receptor (EBVR) for Epstein Barr virus (EBV). Isolated fluid-phase CR2 bound to C3d on erythrocytes (EC3d) and inhibited both B cell-EC3d rosettes and the agglutination of EC3d by anti-C3d, it failed to inhibit either the binding or superinfection of B cells by EBV. By contrast, isolated fluid-phase EBVR inhibited EBV B cell binding activity and superinfection but had no CR2 activity. In addition, radiolabeled CR2 bound to EC3d and anti-CR2-Sepharose, whereas radiolabeled EBVR did not. Purified fluid-phase C3d fragments inhibited EC3d rosette formation with CR2+/EBVR+ cells but did not inhibit EBV binding. However, EBV binding to B cells did inhibit EC3d rosette formation. Clones of human/mouse somatic cell hybrids made from CR2+/EBVR+ human B lymphoblastoid cell and CR2-/EBVR- mouse myeloma cell parents expressed either EBVR or CR2 but only rarely expressed both EBVR and CR2. This suggested that the genes for EBVR and CR2 were located on two different human chromosomes. Thus it was concluded that CR2 is probably not the binding site for EBV.

Animals↗

PubMed1993

Complement and the recruitment of mononuclear osteoclasts.

AIM: To investigate the hypothesis that complement mediates the recruitment of mononuclear osteoclast precursors to the exposed mineralised bone surface. METHODS: Synthetic hydroxyapatite was incubated in vitro with fresh human serum, with and without complement activation inhibitors. Assays for complement components and the generation of the C3 breakdown product C3d were done. C3 deposition in human fetal tibia primary spongiosa was localised immunohistochemically and complement receptors CR1, CR2, CR3, and CR4 were localised cellularly. Immunohistochemical and enzyme histochemical characterisation of the mononuclear and multinuclear osteoclasts was made with emphasis on their association with complement C3 deposition. RESULTS: Components of complement bind to synthetic hydroxyapatite crystals and, at lower concentrations, C3d was generated in the fluid phase. C3 was deposited in a focal and linear distribution on newly formed bone trabecular surfaces in the primary spongiosa. In a similar distribution CD61, CD68, and tartrate resistant acid phosphatase positive mononuclear osteoclasts were shown in close apposition to the bone trabecular surface. These mononuclear osteoclasts, unlike multinucleate osteoclasts, expressed the complement receptors CR3 and CR4. CR1 and CR2, however, could not be shown on either mononuclear or multinuclear osteoclasts. CONCLUSION: It is suggested that C3 deposition on mineralised bone surfaces mediates the recruitment of mononuclear osteoclasts to this site. As the mononuclear osteoclasts fuse to form the multinucleate osteoclast, complement receptor expression is lost.

Bone Development↗

PubMed1998

Platelet adhesion onto artificial surfaces: inhibition by benzamidine, pentamidine, and pyridoxal-5-phosphate as demonstrated by flow cytometric quantification of platelet adhesion to microspheres.

An appreciable effort is directed toward designing strategies to minimize platelet interactions with artificial surfaces, because their reactivity is thought to promote thrombus formation and lead to materials failure. Although platelet glycoprotein Ib/IX (GPIb/IX) and glycoprotein IIb/IIa (GPIIb/IIIa) receptors are thought to mediate adhesion, whether GPIIb/IIIa receptors are activated and how this might occur are largely unknown and are the focus of this article. There are a few ways, other than thrombin generation, that blood contact with artificial surfaces can lead to GPIIb/IIIa activation. Complement activation can lead to products capable of activating platelets (C1q, C5b-9), and contact between platelet CD32 (FcgammaRII) receptors and immobilized immunoglobulin G could also activate platelets. In this article the potential role of these processes was evaluated by using various inhibitors in a microsphere-based platelet adhesion immunoassay. Polystyrene microspheres (10 microm) were incubated in platelet-rich plasma before flow cytometric analysis of beads for adherent platelets. The data eliminated occupancy of the FcgammaRII receptor (by use of IV.3 blocking antibody), C5b-9 production (by use of sCR1), and the indirect action of factor XIIa on complement components (by use of corn trypsin inhibitor) as playing roles in supporting platelet adhesion. Agents directed against the first complement component (benzamidine, pentamidine, pyridoxal-5-phosphate) were effective inhibitors of platelet adhesion and were also demonstrated to inhibit SC5b-9 and C3d levels on the bead surface after serum incubations. Because these agents are not highly specific, it can not be concluded that C1q is a mediator of adhesion. These agents were also demonstrated to inhibit fluorescein isothiocyanate-fibrinogen binding to activated washed platelets, therefore indicating that fibrinogen receptor expression is a requirement for platelet adhesion.

Benzamidines↗