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PubMed1988

The phagocytic activity of Lumbricus terrestris leukocytes is enhanced by the vertebrate opsonins: IgG and complement C3b fragment.

The effect of the vertebrates opsonins: IgG and complement C3 fragments on phagocytic activity of Lumbricus terrestris leukocytes towards sheep erythrocytes was studied. Sheep erythrocytes were previously sensitized with specific IgG or IgM and coated with one of the third component fragments (C3b, C3bi, C3d) of human complement. Our results show that leukocyte phagocytosis was enhanced by vertebrate IgG and C3b complement fragments but not by IgM and fragment C3d. Because opsonization in vertebrates is related to the presence of receptors on the surface of phagocyte membrane, our results suggest that similar receptors exist on earthworm leukocyte surfaces. These new data strengthen the arguments in favour of the presence of components in Lumbricus terrestris which partially share common structures and functions with components of vertebrate humoral immune reactions.

Animals↗
PubMed1998

Complement activation during major surgery: the effect of extracorporeal circuits and high-dose aprotinin.

OBJECTIVE: To assess the in vivo contribution to complement activation of an extracorporeal circuit and the use of high-dose aprotinin during major surgery. DESIGN: Sequential samples were obtained from 8 patients undergoing thoracic surgery, 20 patients undergoing orthotopic liver transplantation (OLT) using venovenous bypass, and 19 patients undergoing cardiac surgery using cardiopulmonary bypass (CPB). INTERVENTION: The latter two groups were part of a randomized controlled trial of high-dose aprotinin. MEASUREMENTS: Total complement activation was measured with the hemolytic complement activity and the C3 activation-specific marker, C3d antigen. MAIN RESULTS: Complement activation did not occur during thoracic surgery. During OLT, C3d antigen levels, expressed as mean +/- standard deviation (SD), were elevated from baseline at skin closure (8.6 +/- 2.5 v 13.0 +/- 5.2 mg/L; p = 0.0082). During cardiac surgery, C3d antigen levels increased 10 minutes after the start of CPB (pre-CPB, 8.0 +/- 1.9 v 14.2 +/- 3.1 mg/L; p = 0.0001) and remained at greater than baseline values postoperatively (8.0 +/- 1.9 v 11.8 +/- 2.3 mg/L; p = 0.002). There was no difference in complement activation in those receiving high-dose aprotinin during OLT or cardiac surgery. Complement activation during cardiac surgery using extracorporeal circulation occurred to a greater extent than during OLT and thoracic surgery. Complement activation during cardiac surgery or OLT was not attenuated by the use of high-dose aprotinin.

Adolescent↗
PubMed1989

Complement components in Nigerians with bronchial asthma.

Serum complement components C1q, C3, C4, factor B, and C3d breakdown products were measured in asthmatic Nigerians and in age-matched and sex-matched controls. C3 mean level was higher than in controls while C1q and C4 mean levels were lower than in controls. High levels of C3d in asthmatic patients suggest the possible role of C3a and C5a anaphylatoxins in the etiopathogenesis of perennial asthma in Nigerian patients in a tropical environment with ubiquitous airborne allergens and infective agents. The significantly elevated levels of IgM and IgG may suggest recurrent respiratory challenge of perennial antigens in our environment.

Adult↗
PubMed1999

Functional properties of complement factor H-related proteins FHR-3 and FHR-4: binding to the C3d region of C3b and differential regulation by heparin.

The human factor H-related proteins FHR-3 and FHR4 are members of a family of proteins related to the complement factor H. Here, we report that the two proteins bind to the C3d region of complement C3b. The apparent K(A) values for the interactions of FHR-3 and FHR-4 with C3b are 7.5 x 10(6) M(-1) and 2.9 x 10(6) M(-1), respectively. Binding studies performed with C3b-coated pneumococci confirmed the results obtained with the biosensor system. A C-terminal construct of factor H showed similar binding characteristics. The interaction of FHR-3, but not of FHR4, with opsonised pneumococci was inhibited by heparin.

Apolipoproteins↗
PubMed1983

Comparison of different assays for circulating immune complexes in age matched vasectomized and non-vasectomized men.

Sera from 46 men vasectomized for 5 yr and from 46 age-matched nonvasectomized men had previously been analyzed for circulating immune complexes (CICs) by four assays. Four additional CIC assays have now been performed on these sera: three Raji cell enzyme-linked immunosorbent assays (ELISAs) using alkaline phosphatase-conjugated antihuman IgG, IgA or C3 and the bull sperm ELISA. No significant differences in CIC levels were detected between the two groups using any of the assays. Results for two different sera obtained from 16 men 4 1/2 months apart correlated significantly for six of seven CIC assays evaluated in this way. In the bull sperm and Raji cell ELISAs, utilizing anti-IgG in the detection layer, the vasectomized men with sperm-agglutinating antibodies were found to have significantly higher CIC levels than those without sperm agglutinants. No association was found between the presence of sperm protamine antibody and levels of CICs. Since the vasectomized and control groups did not differ with respect to levels of CICs, immunoglobulins, or the complement C3 split product C3d, all 92 samples were combined into one group for further analysis. Serum IgG levels significantly correlated with the CIC levels in four of five CIC assays involving binding of IgG; IgA levels correlated with CIC determinations in the Raji-IgA assay, while plasma C3d levels correlated with the Raji-C3, the Raji-IgA, and the C1q-protein A binding assays. IgM levels did not correlate with activity in any assay. Finally, the degree of correlation between all eight CIC assays was determined, and significant positive correlations between assays were found in ten of twenty-eight comparisons.

Adult↗
PubMed1988

Cardiovascular function and arterial blood gases during sham dialysis in healthy man.

Cardiovascular function and alveolar gas exchange were studied in healthy subjects undergoing sham dialysis (SHD)--i.e. the circulation of blood through a cuprophane dialyzer with the dialysate compartment closed to avoid diffusion and convective transport of fluid and solutes. The blood-membrane contact induced complement activation (rise in C3d) and transient leukopenia, as described during clinical hemodialysis. PaO2, PaCO2 and calculated oxygen uptake remained unchanged. Heart rate, cardiac index (thermodilution), systemic vascular resistance index and brachial and pulmonary arterial blood pressures did not change significantly during 150 min of SHD (n = 8). In 12 subjects, in whom more frequent measurements were made during the first 30 min of SHD, pulmonary arterial systolic and diastolic blood pressures decreased significantly while the dialyzer and the tubing set filled with blood, and pulmonary arterial mean blood pressure did not change significantly. Pulmonary capillary wedge pressure fell during the filling phase, but did not change significantly during SHD; pulmonary vascular resistance index remained unchanged. We conclude that in nonuremic subjects sham dialysis with a cuprophane dialyzer does not result in hypoxemia, pulmonary vascular constriction and pulmonary hypertension, in spite of complement activation and marked leukopenia.

Acid-Base Equilibrium↗
PubMed1985

Platelet associated complement components (PAC3c and PAC3d) in patients with autoimmune thrombocytopenia.

Platelet associated C3c and C3d (PAC3c and PAC3d) were quantitated by enzyme linked assay in 105 patients with idiopathic autoimmune thrombocytopenia (AITP) in whom elevated platelet associated immunoglobulins (IgG and IgM) had previously been documented. Increased levels of complement components were demonstrated in 46 of 105 patients (43.8%). In 11 of these patients, PAC3d alone was abnormal implying that C3b had been inactivated after cleavage by C3 inactivator in vivo. Complement binding was seen in two of 16 patients (12.5%) with raised PAIgG alone, four of 19 patients (21.0%) with raised PAIgM alone and in 40 of 70 patients (57.1%) in whom PAIgG and PAIgM were raised together. This difference was highly significant (P = 0.01). The clinical implication of these findings are discussed.

Autoimmune Diseases↗
PubMed1995

Evidence for activation of the terminal pathway of complement and upregulation of sulfated glycoprotein (SGP)-2 in the hypoglossal nucleus following peripheral nerve injury.

In a previous study, we found immunoreactivity for complement factors C3, C3d, and C4d, as well as endogenous IgG in the hypoglossal nucleus following hypoglossal nerve transection, suggesting that activation of the complement cascade had taken place in the vicinity of the axotomized motorneurons. In the present study, we found increased immunoreactivity for complement factor C1 and C1q in reactive microglia, indicating an increased potential for initiation of the classical pathway by binding of IgG to C1q. Furthermore, we found immunoreactivity for C9, which contributes to the formation of C5b-9, the final lytic product of the complement cascade close to the axotomized neurons and perineuronal glia. In addition, immunoreactivity and mRNA labeling of sulfated glycoprotein (SGP-2), a putative complement inhibitor, was increased in a subpopulation of the axotomized motorneurons. SGP-2 immunoreactivity was also increased in astroglial cells ipsilateral to the nerve injury. The results lend further support to the hypothesis that the complement cascade is activated in the vicinity of axotomized neurons, which in turn may be protected by complement inhibitors. The balance between activation of complement and complement inhibitors might have an impact on the degenerative components of the axon reaction and, in particular, the events leading to nerve cell death.

Animals↗
PubMed1993

Why do patients develop reactions to streptokinase?

Minor reactions to streptokinase are not uncommon, although the etiology is unknown. It is widely presumed, however, that these, like the more serious immune reactions, are antibody-mediated. We measured specific anti-streptokinase IgG, subclasses IgG1, IgG2, IgG3, IgG4 and IgE by ELISAs, haemagglutination, indirect Coombs' test and immunoblotting in six patients who developed reactions to streptokinase. Evidence of complement activation by streptokinase was sought by a haemolytic complement assay and by measurement of C3, C4 and C3d. The patients who reacted to streptokinase presented with low titres of anti-streptokinase IgG (median = 5; range 0-32) and IgG1 (median = 3; range 0-14). No evidence of any other IgG subclass was found, nor of specific anti-streptokinase IgE. Anti-streptokinase IgG1 was found to fix complement; patients who reacted to streptokinase were found to have low levels of total complement 1 year post reaction. Probable aggregates and fragments of human albumin (added stabilizer) were found in the streptokinase preparation and proved to be antigenic in some patients, but were not found to be related to the development of reactions. The findings suggest that patients who develop reactions to streptokinase cannot be predicted on the basis of antibody titres at presentation. Minor reactions to streptokinase would not appear to be antibody-mediated, although complement activation may be involved.

Aged↗
PubMed1994

Complement activation by recombinant HIV-1 glycoprotein gp120.

The mechanism of CD4+ cell depletion in HIV-infected patients is poorly understood. In this study we investigated whether rgp120 can activate the complement system in the absence of anti-gp120 Abs. We found that the complement proteins C4, C3d, C5b-9, and properdin bind to rgp 120-coated CD4+ T cells of healthy individuals when incubated in autologous serum. Activation of the complement system occurred primarily via the classical pathway and was abolished in sera deficient in C1q and C4 as well as in the presence of EDTA. No cell lysis was observed in a lymphocytotoxicity assay using human serum, possibly because of homologous restriction of complement lysis. In contrast, addition of rabbit sera induced lysis of the rgp 120-precoated cells. Cell lysis by rabbit serum was found to be because of naturally occurring IgM anti-gp 120 Abs. The rgp 120, which was immobilized on the surface of microtiter plates activated complement in the absence of lymphocytes. Complement activation by cell-bound HIV-1 envelope glycoprotein gp120 with subsequent opsonization may be relevant for the elimination of noninfected CD4+ T cells in HIV-infected patients.

Amino Acid Sequence↗
PubMed1998

Interaction of vaccinia virus complement control protein with human complement proteins: factor I-mediated degradation of C3b to iC3b1 inactivates the alternative complement pathway.

Vaccinia virus complement control protein (VCP) is a virulence determinant of vaccinia virus that helps protect the virus from the complement attack of the host. To characterize the interaction of VCP with C3 and C4 and understand the mechanism by which VCP inactivates complement, we have expressed VCP in a yeast expression system and compared the biologic activity of the purified protein to that of human factor H and complement receptor 1 (CR1). Recombinant VCP bound to C3 and the proteolytically cleaved form of C3 (C3b), but not to the 135,300-m.w. fragment of C3 generated using elastase (C3c) and the 35,000-m.w. fragment of C3 generated using elastase (C3d) and inhibited both the classical and alternative pathways of complement activation. Although rVCP was less effective at inhibiting the alternative pathway than factor H or CR1, it was more effective than factor H at inhibiting the classical pathway. Unlike factor H, rVCP was unable discriminate between alternative pathway-mediated lysis of rabbit and sheep E. A comparison of the cofactor activity in factor I-mediated cleavage of C3b suggested that in contrast to factor H and CR1, which displayed cofactor activity for the three sites, rVCP displayed cofactor activity primarily for the first site, leading to generation of C3b cleaved by factor I between Arg1281-Ser1282 (iC3b1). Its cofactor activity for C4b cleavages was similar to that of soluble complement receptor type 1. Purification and functional analysis of iC3b1 showed that it was unable to interact with factor B to form the alternative pathway C3 convertase, C3b,Bb. These results suggest that the interaction of VCP with C3 is different from that of factor H and CR1 and that VCP-supported first cleavage of C3b by factor I is sufficient to render C3b nonfunctional.

Arginine↗
PubMed1993

Analysis of mannoproteins from blastoconidia and hyphae of Candida albicans with a common epitope recognized by anti-complement receptor type 2 antibodies.

Mannoproteins of approximately 50 kDa from blastoconidia and 60 kDa from hyphae of Candida albicans reacted in Western blots (immunoblots) with either a polyclonal rabbit antiserum (CA-7) or a monoclonal antibody (CA-A) to the C. albicans C3d-binding protein (complement receptor type 2). The glycosylated nature of these proteins was demonstrated by their reactivity with concanavalin A and by selective labeling with the biotin-hydrazide reagent following periodate oxidation. Differences in the oligosaccharides of these proteins were observed in regard to their reactivity with lectin-peroxidase reagents and sensitivity to glycosidases such as N-glycanase or endoglycosidase F (but not endoglycosidase H). The 60-kDa mannoprotein reacted with wheat germ agglutinin, while the 50-kDa mannoprotein did not. Treatment of the 60-kDa mannoprotein with the glycosidases mentioned above resulted in its conversion into a species of 40 to 45 kDa. Enzyme treatment had no obvious effect on the electrophoretic mobility of the 50-kDa species from blastoconidia. Both the 50- and 60-kDa glycoproteins remained immunoreactive after treatment with the glycosidases. Reactivities of the two mannoproteins to neuraminidase also differed. Finally, the 50-kDa (blastoconidia) and the 60-kDa (hyphae) mannoproteins were purified by using ion-exchange chromatography and electroelution. The purified proteins differed in net charge, the 60-kDa species having a more acidic pI. Functional activity of the purified mannoproteins was demonstrated, as each inhibited the rosetting of antibody-sensitized sheep erythrocytes conjugated with iC3b or C3d by hyphae. Thus, an epitope(s) common to both a mycelial and blastoconidial mannoprotein is associated with a structurally different oligosaccharide for each growth form.

Animals↗
PubMed1978

Membrane receptors of mouse leukocytes. II. Sequential expression of membrane receptors and phagocytic capacity during leukocyte differentiation.

Analysis of four mature cell markers on mouse bone marrow leukocytes grown in vitro, demonstrated a distinct sequence of marker appearance during the terminal phases of granulocytic cell differentiation. A similar pattern of marker expression was also suggested by analysis of mature neutrophils and macrophages isolated from normal tissues. Among cultured neutrophils, receptors for the Fc portion of IgG (FcR) were first expressed on myelocytes and metamyelocytes, and then subsequently on more mature cells. Morphologically mature colony neutrophils (polymorphs) from agar cultures contained only FcR and complement receptor type two (CR(2)) (C3d receptor), and lacked both complement receptor type one (CR(1)) (C3b receptor) and the capacity to ingest latex, bacteria, or iron particles. Neutrophils from 2 and 3 wk liquid media cultures of marrow cells differed from agar grown neutrophils in that they had phagocytic capacity (particle ingestion) [Pi] in addition to FcR and CR(2). Furthermore, in the 4th and 5th wk of these continuous liquid cultures, CR(1) was also expressed, completing the surface marker profile of normal blood neutrophils. Based on these studies, the following order of appearance of these four markers on cells from the myelocytic series was proposed: FcR {arrow} FcR CR(2) {arrow} FcR CR(2) Pi {arrow} FcR CR(2) Pi CR(1). Differential studies of tissue leukocytes containing these same markers revealed that a heterogeneity existed among morphologically mature neutrophils. Even though 95 percent of blood polymorphs contained all four markers, the same was true of only half of spleen polymorphs and only 20 percent of bone marrow polymorphs. Cells of the monocyte-macrophage series were studies in parallel with neutrophils. Cultured marrow monocytes acquired the four mature cell markers so rapidly that the order of receptor appearance could not be determined. However, it was found that CR2 was lost during the terminal phase of monocyte maturation into activated macrophages.

Animals↗
PubMed1998

C4AQ0 superimposed on a primary defect increases the susceptibility to systemic lupus erythematosus (SLE) in a family with association between C4AQ0 and SLE.

OBJECTIVE: To investigate the association of C4AQ0 with increased incidence of systemic lupus erythematosus (SLE) or positive serology (28%) in an extended Icelandic family, and whether this can be explained by impaired complement function in handling immune complexes (IC). METHODS: The ability of the classical pathway to opsonize nascent IC [alkaline phosphatase (AP)-anti-AP] and bind them to human erythrocytes was evaluated by the new ICRB assay. The capacity of erythrocytes from family members to bind nascent IC was also measured by a modification of the ICRB assay. IC levels were measured by complement consumption assay, C3d by a sandwich ELISA, factor B by immunoelectrophoresis, and the alternative pathway function by a hemolytic assay. RESULTS: Family members with homozygous or heterozygous C4AQ0 (47%) showed no impaired complement dependent opsonization of IC and binding to erythrocytes. Their factor B and alternative pathway function was normal. Fifty-six percent of the family members (n=18) had abnormally high IC levels, seemingly independent of C4AQ0. However, 6 of the 7 individuals with high IC levels and SLE symptoms had C4AQ0 compared to 2 of 11 symptom-free individuals with high IC levels. CONCLUSION: Our results suggest that the susceptibility for SLE in this family may result from 2 different defects, one leading to elevated IC levels, and another associated with C4AQ0 without detectable impairment in the complement dependent IC transport mechanism. Individuals with both abnormalities have increased susceptibility to SLE.

Antigen-Antibody Complex↗
PubMed1983

Acute complement activation during an anaphylactoid reaction to blood transfusion and the disappearance rate of C3c and C3d from the circulation.

A patient experienced an anaphylactoid shock after receiving a transfusion with 5-10 ml of leucocyte-depleted blood. Complement measurements revealed pronounced elevation of split products of the third complement factor (C3c and C3d), normal but fluctuating levels of native C3, significantly decreased levels of C4, normal factor B concentrations and low levels of factor B split products. The results indicate complement activation via the classical pathway as a causative mechanism of the anaphylactoid shock, and suggest an antigen-antibody reaction as the etiological factor. The nature of the antigen-antibody reaction initiating the complement activation could not be established. The disappearance rate (T/2) of C3d from the plasma after the acute C-activation was measured to approximately 4 hr, and the half life of C3c was significantly shorter.

Adult↗
PubMed1982

The complement fixing ability of putative circulating immune complexes in rheumatoid arthritis and its relationship to extra-articular disease.

The hypothesis that the pathogenicity of putative circulating immune complexes (CIC) in rheumatoid arthritis (RA) is related to their ability to fix complement was investigated. Three assays for CIC were employed; (a) the 125I C1q binding assay (C1q BA), (b) the C1q solid phase assay (C1q SP) and (c) the Raji cell assay (RCA). Evidence for hypercatabolism of complement was obtained by using a highly sensitive quantitative assay for C3d (a breakdown product of C3) by rocket immunoelectrophoresis. One hundred and fifty-two patients with classical or definite RA were studied; 54 had clinical evidence of extra-articular disease including vasculitis, nodules, scleritis, neuropathy and lung disease; 98 patients had clinical evidence of joint disease alone. Plasma levels of C3d were significantly elevated in the RA group as a whole 16.7 +/- 4.4 mg/l (mean +/- 1 s.d.) compared with 13.1 +/- 3.25 mg/l in a group of 55 normal controls (P less than 0.01). Elevated levels of C3d were found in 26% of all patients but occurred significantly more often in the extra-articular disease group (P less than 0.05). Fifty-four percent of patients had at least one positive assay for CIC although no individual assay was positive in more than 36% of the group as a whole. The prevalence of positive CIC was significantly greater in those patients with extra-articular disease than in those with joint disease alone (P less than 0.005). Of the total of 82 patients with putative CIC, 30 (37%) had a raised C3d level. The coincident finding of positive tests for CIC and an elevated C3d level was very significantly correlated with the presence of extra-articular disease (chi 2 = 12.7 P = 10(-3)). Whilst putative CIC are frequent in RA (54%) these findings in contrast to previous work, suggest that the majority are not associated with abnormal complement activation and may account for the relative infrequency of clinically detectable active extra-articular disease.

Adolescent↗
PubMed1994

Activity and activation of the complement system in patients being operated on for cancer of the colon.

OBJECTIVE: To find out if there was any local activation of complement in the vicinity of a colonic cancer, and any fluctuation in the function of the complement system during operation. DESIGN: Prospective study. SETTING: One university and two district hospitals in Denmark. SUBJECTS: 29 selected patients undergoing emergency and elective operations for colonic cancer. INTERVENTIONS: Measurements of systemic and local complement fixation capacity and complement activation in samples of serum or plasma taken before, during, and after operation. MAIN OUTCOME MEASURES: Changes in complement fixation capacity and complement activation during operation. RESULTS: Haemodilution during operation caused a significant reduction in the complement fixation capacity of serum and in the activation of the complement system as measured by generation of C3c. We were unable to confirm the presence of complement inhibitors during operation. Haemodilution caused a 30% reduction in fixation capacity of C3b (12/29 samples of serum had values more than 2SD below the mean of the reference range compared with 4/29 before operation). The activity of C4 was reduced by 25% during operation and the capacity of the complement system to fix C3b and C4b was restored to baseline nine days postoperatively. Concentration of C3d was significantly higher in serum from tumour venous blood compared with that from peripheral blood during operation. CONCLUSION: The presence of complement activation products in the general circulation reflects local activation of the complement system in the vicinity of the tumour, but this may have been influenced by tissue necrosis or subclinical infection. Haemodilution causes a significant reduction in the capacity of the complement system during operation, whereas inhibitory factors associated with the cancer or operation and anaesthesia could not be demonstrated. We found no correlation between complement activity and clinical data.

Adult↗
PubMed1983

Classical pathway activation during an adverse response to protamine sulphate.

A severe anaphylactoid reaction was observed following the i.v. administration of protamine sulphate in a 66-year-old male undergoing coronary artery catheterization. Serial measurements of complement factors (C3 and C4) and C3 split products (C3c and C3d) were performed by conventional electro-immunoassays and by double zone rocket immunoelectrophoresis. A parallel decrease in circulating C3 and C4 concentrations was seen for 1 h, reaching a nadir at 1.3 h. Markedly increased concentrations of C3c and C3d were observed in the first sample examined after exposure to the drug. C3c and C3d concentrations gradually declined to the normal range within 5.9 h and 21.8 h, respectively. These observations are discussed in relation to the mechanism of this adverse reaction.

Aged↗