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PubMed1998

Reference typing report for complement component C3.

A comparison of five C3 variant samples has been performed by conventional high-voltage gel electrophoresis in three laboratories (Palermo, Berlin and Mainz). Local designation was shown within SD = +/-0.75 mm migration distance in the Mainz laboratory. Methodological modifications by laboratories were not accounted for (cooling temperature, relative mobilities between runs). In parallel, all reference samples were also sequenced after exon-specific amplification. As a result, two variants with identical final designations and two variants with different mobilities were shown to conform at the molecular basis exhibiting an amino acid exchange that causes the corresponding change in relative mobility as compared to normal C3F and C3S.

Blood Protein Electrophoresis↗

PubMed1983

Deposits of immunoglobulins and complement factor C3 in human dental periapical inflammatory lesions.

Thirty-five human dental periapical lesions were studied by immunofluorescence technique using polyclonal anti-IgG (F(ab)2), anti-IgM (F(ab)2), anti-IgA (F(ab)2), anti-IgE and anti-C3c as well as monoclonal anti-IgE. Prewashed ethanol-fixed specimens showed a great number of plasma cells staining for IgG. Cells containing IgA, IgM or IgE were also seen. Deposits of immunoglobulins and C3c suggestive of immune complexes were demonstrated using a double staining technique combining FITC-labeled immunoglobulins with TRITC-conjugated C3c. The complexes were located intracellularly in macrophages, as well as in vessel walls and in the basement membrane zone of proliferating epithelium. Immune complexes may be involved in the epithelial proliferation in those granulomas which lead to cyst formation. Monoclonal anti-IgE demonstrated plasma cells and mast cells, as well as intercellular IgE in epithelial strands of granulomas. The role of IgE in the epithelium is obscure. The study strongly indicates the involvement of hypersensitivity reactions type I and III in periapical inflammatory lesions.

Adult↗

PubMed2003

Mobilization studies in mice deficient in either C3 or C3a receptor (C3aR) reveal a novel role for complement in retention of hematopoietic stem/progenitor cells in bone marrow.

The mechanisms regulating the homing/mobilization of hematopoietic stem/progenitor cells (HSPCs) are not fully understood. In our previous studies we showed that the complement C3 activation peptide, C3a, sensitizes responses of HSPCs to stromal-derived factor 1 (SDF-1). In this study, mobilization was induced with granulocyte colony-stimulating factor (G-CSF) in both C3-deficient (C3-/-) and C3a receptor-deficient (C3aR-/-) mice as well as in wild-type (wt) mice in the presence or absence of a C3aR antagonist, SB 290157. The data indicated (1) significantly increased G-CSF-induced mobilization in C3-/- and C3aR-/- mice compared with wt mice, (2) significantly accelerated and enhanced G-CSF-induced mobilization in wt, but not in C3-/- or C3aR-/-, mice treated with SB 290157, and (3) deposition of C3b/iC3b fragments onto the viable bone marrow (BM) cells of G-CSF-treated animals. Furthermore, mobilization studies performed in chimeric mice revealed that wt mice reconstituted with C3aR-/- BM cells, but not C3aR-/- mice reconstituted with wt BM cells, are more sensitive to G-CSF-induced mobilization, suggesting that C3aR deficiency on graft-derived cells is responsible for this increased mobilization. Hence we suggest that C3 is activated in mobilized BM into C3a and C3b, and that the C3a-C3aR axis plays an important and novel role in retention of HSPCs (by counteracting mobilization) by increasing their responsiveness to SDF-1, the concentration of which is reduced in BM during mobilization. The C3a-C3aR axis may prevent an uncontrolled release of HSPCs into peripheral blood. These data further suggest that the C3aR antagonist SB 290157 could be developed as a drug to mobilize HSPCs for transplantation.

Animals↗

PubMed1985

C3 and C6 complement types in schizophrenia.

C3 and C6 complement types were studied in schizophrenic patients and controls. The distributions of the three common C3 types (F, FS and S) among the patients was significantly different from that in the controls (p less than 0.005) and the frequency of the C3F gene was significantly increased (p less than 0.0005) among the patients. There were no significant differences in C6 gene or phenotype frequencies between patient and controls.

Complement C3↗

PubMed1983

Immunologic studies of human schistosomiasis. I. Clinical and immunological findings in acute and chronic schistosomiasis.

Sera and ascitic fluid of 26 patients with acute and chronic schistosomiasis were studied for the presence of circulating immune complexes (CIC's), IgG, IgM, IgA, complement C3 and C4, as well as their correlation with the clinical manifestations of the disease. Serum levels of CIC's and IgG were significantly increased in patients with acute S. mansoni and S. haematobium infections and in patients with chronic schistosomiasis. Serum IgA levels were evaluated in 20% of patients with S. mansoni infection, 67% with S. haematobium infections and in 100% of chronically infected patients. Complement C3 levels were normal in all patients. Ascitic fluid analysis revealed the presence of IgG, IgM, IgA, C3 and C4 and high concentrations of CIC's. A significant positive correlation was demonstrated to occur between serum CIC's and IgG, as well as between the serum and ascitic fluid levels of CIC's of chronic patients. These findings also correlated with the degree and severity of the clinical syndrome.

Acute Disease↗

PubMed1996

Acute phase proteins in male Chinese schizophrenic patients in Singapore.

Changes in the concentration of some serum acute phase proteins (alpha 1-antitrypsin, alpha 2-macroglobulin, complement C3, haptoglobin, ceruloplasmin, transferrin, albumin and hemopexin), thyroxine-binding globulin, retinol-binding globulin, plasminogen and Gc-globulin are reported in two separate series of Chinese, male schizophrenic patients and healthy controls. In the first series, 41 healthy blood donors and 98 schizophrenic patients in different stages of the disease were investigated. The second series consists of a random sample of 50 acutely ill schizophrenic patients and a second group of healthy subjects. The concentrations of these serum proteins were measured by rocket immunoelectrophoresis in agarose gel. Increased levels of serum alpha 1-antitrypsin, alpha 2-macroglobulin, haptoglobin, ceruloplasmin, and thyroxine-binding globulin were observed in both series of patients when compared to their respective controls. Albumin, transferrin and retinol-binding protein levels were reduced in patients in both series. Hemopexin levels were increased only in the acutely ill patients while complement C3 was decreased in the chronically ill patients. No changes were observed in the Gc-globulin levels of all groups of patients. With the exception of complement C3, the changes observed in the levels of these serum proteins were appropriate for that of an acute phase response.

Acute Disease↗

PubMed1986

Tropical pyomyositis: is it an immunodeficiency disease?

Serum immunoglobulin (IgG, IgM, IgA) and complement (C3, C4) levels were measured by radial immunodiffusion technique in a group of 16 Nigerian patients with tropical pyomyositis (TP). Sixteen healthy Nigerians, age- and sex-matched with the patients, were also included in the study as control subjects (CS). A significantly low level of circulating IgM (P less than 0.01) and elevation of the serum levels of IgG (P less than 0.01) and IgA (P less than 0.01) were observed in TP compared to CS. Mean serum complement (C3, C4) levels were found to be similar in patients and controls. Microbiological culture tests showed that 14 pus specimens (88%) and 3 blood specimens (19%) from the patients were positive for Staphylococcus aureus. It was therefore proposed that IgM antibody deficiency (primary or acquired) against S. aureus may be the cause of tropical pyomyositis in Nigerians.

Adolescent↗

PubMed1990

Longitudinal study of proteins in plasma and dialysate during continuous ambulatory peritoneal dialysis (CAPD).

The aim was to evaluate plasma proteins during continuous ambulatory peritoneal dialysis (CAPD) in relation to dialysis losses, membrane permeability, renal insufficiency, and time on CAPD. Ten male patients, established on CAPD for at least 14 months, were studied every 8 weeks for 56 weeks. Blood and dialysate from the morning exchange were analysed for urea, creatinine, and 7 proteins, and used to calculate dialysate to plasma concentration ratios (D/P). These ratios were not significantly changed suggesting that permeability remained constant. However, there was a trend for beta 2-microglobulin, creatinine, and urea to increase progressively. After 56 weeks, beta 2-microglobulin had increased from 27.9 to 31.3 mg/L (p less than 0.05) and creatinine 1006 to 1099 mumoL/L (p less than 0.05) and both correlated with time on CAPD (p less than 0.001). Plasma alpha 1-acid glycoprotein, albumin, transferrin, IgG, IgA, and complement C3 were not significantly changed, although IgA and complement C3 were each negatively correlated with time on CAPD (r = -0.70 and -0.67, respectively), creatinine (r = 0.51 and -0.54), and urea (r = -0.61 and -0.61) (p less than 0.001 for all). It is concluded that increases in beta 2-microglobulin, creatinine, and urea are not due to loss of membrane permeability but reflect a slight increase in uraemia. Long-term decreases in immunological proteins may be caused by uraemia or progressive depletion.

Adult↗

PubMed1988

Alpha- and gamma-interferon (IFN alpha, IFN gamma) but not interleukin-1 (IL-1) modulate synthesis and secretion of beta 2-microglobulin by hepatocytes.

Soluble serum beta 2-microglobulin has been thought to result from membrane shedding by activated T-lymphocytes. This hypothesis could explain the increase of beta 2-microglobulin serum levels during virally induced mononucleosis, but not elevated levels as observed in other virally induced and in malignant diseases. In this paper we demonstrate that beta 2-microglobulin is a true secretory protein, and that its synthesis in hepatocytes is modulated by IFNs but not by IL-1. While the 45,000 MW HLA antigen can be found only in cell lysates, beta 2-microglobulin is shown to be secreted also into the culture medium like other secretory proteins (e.g. albumin-factor B-complement C3). Furthermore, interferon alpha (IFN alpha) as well as interferon gamma (IFN gamma) directly stimulate, in a dose- and time-dependent manner, beta 2-microglobulin synthesis by human hepatoma cells (Mz-Hep-1 and PLC/PRF5) and murine hepatocyte primary cultures. The increase of beta 2-microglobulin production induced by interferons is demonstrated at both the protein and the RNA level, indicating that interferon acts at a pretranslational level. The interferon effect on beta 2-microglobulin synthesis is specific since synthesis of secretory proteins like complement C3 or albumin, and of a structural protein like actin, remains unchanged. In contrast to IFN, IL-1, the main mediator of acute phase response, does not change beta 2-M biosynthesis rate. These data indicate that (i) beta 2-microglobulin is a secretory protein, (ii) IFNs but not IL-1 can mediate increased beta 2-M serum levels, and (iii) the liver may be its primary source.

Albumins↗

PubMed2000

Local neutrophil influx following lateral fluid-percussion brain injury in rats is associated with accumulation of complement activation fragments of the third component (C3) of the complement system.

Traumatic brain injury can lead to locally destructive secondary events mediated by several inflammatory components. Following lateral fluid-percussion (FP) brain injury in rats, we examined cortical and hippocampal sections for neutrophil infiltration and accumulation of complement component C3. Neutrophil influx into the brain after injury was detected by an improved myeloperoxidase (MPO) microassay and manual cell counting, while C3 accumulation was detected using immunocytochemistry. MPO levels were elevated in the injured cortical tissue, whereas C3 immunoreactivity was increased in both injured cortical and ipsilateral hippocampal sections. These results show that the FP model of head injury leads to an intense local inflammatory reaction and subsequent tissue destruction.

Animals↗

PubMed1983

Human peripheral blood monocyte-derived macrophages produce haemolytically active C3 in vitro.

The third component of complement (C3) synthesized by human monocyte-derived macrophages has been shown to have the same size and sub-unit structure as serum C3, but haemolytic activity has not been demonstrated. Human monocyte-derived macrophages were cultured from days 4 to 7 in medium without serum, and the conditioned medium was dialysed to remove inhibitors of the C3 assay and concentrated to enhance detection of low amounts of C3. Using these techniques C3 activity was detected routinely. The amount of C3 was 3.4 x 10(7) effective C3 molecules/ml of concentrated tissue culture medium (range 1.0-7.5 x 10(7)), and the number of C3 molecules synthesized by each cell was 4.4 x 10(5), assuming that each cell synthesized C3. The specific activity of the C3 synthesized by the monocytes was the same as the specific activity of C3 that had been purified from serum and then incubated with the cells and processed in the same manner as the monocyte media. Synthesis as the basis for the presence of the C3 activity in the medium was indicated by an inhibition of production of the C3 activity of 66 +/- 16% by cycloheximide, 2 micrograms/ml. Thus, human blood monocytes that migrate into areas of inflammation can mature into cells capable of producing C3 which can participate in the complement sequence and thus potentiate inflammation.

Cells, Cultured↗

PubMed1990

Participation of C3 and its ligands in complement activation.

C3, the most abundant complement protein in blood, plays a central role in the activation sequence of the complement system as well as in host defense. Expression of the multiple functions of C3 requires its cleavage by highly specific enzymes termed C3 convertases. C3 in a conformationally altered form, C3H2O, resulting from the slow spontaneous hydrolysis of the internal thioester bond of native C3, initiates the assembly of a C3 convertase which continuously cleaves C3 in the blood at slow rates generating a constant supply of small amounts of C3b. When an activator of the alternative complement pathway is present, C3b becomes covalently attached to its surface via an ester or amide bond. Activator surface-bound C3b initiates the assembly of an "amplification" C3 convertase, C3bBb(P), which can efficiently activate C3 and generate additional convertase complexes on the surface of the activator. C3b generated by an amplification or classical pathway C3 convertase can also bind covalently to the noncatalytic subunit, C3b or C4b, respectively, resulting in the generation of a C5 convertase, an enzyme catalyzing the cleavage/activation of C5. In terms of participation in host defense, several fragments of C3, including C3a, C3b, iC3b, and C3dg, mediate a number of important functions such as increased vascular permeability, enhancement of phagocytosis, elimination of immune complexes, and perhaps also proliferative responses and/or differentiation of B cells.

Complement Activation↗

PubMedDate not supplied

Complement proteins and soluble immune complex levels in Nigerians having primary liver cell carcinoma.

Serum Complement (C3), proteins and circulating immune complex levels were estimated in Nigerians having primary liver cell carcinoma and control subjects by immunodiffusion in agar, biuret and polyethylene glycol precipitation methods respectively. The patients were observed to have diminished mean C3 and albumin concentrations whereas the mean total proteins, globulins and soluble immune complex levels were elevated. About 80 percent of the patients who had depressed serum C3 concentrations also had elevated levels of circulating immune complexes. There is however no correlation between the complement (C3) concentrations and the serum levels of immune complexes.

Adolescent↗

PubMed2006

Identification of novel genes regulated by chorionic gonadotropin in baboon endometrium during the window of implantation.

Chorionic gonadotropin (CG) is an early embryo-derived signal that is known to support the corpus luteum. An in vivo baboon model was used to study the direct actions of human CG (hCG) on the endometrium, during the periimplantation period. Endometrial gene expression was analyzed using microarrays. The endometrial biopsies were taken from hCG-treated (n = 5) and control (n = 6) animals on d 10 after ovulation. Class comparison identified 61 genes whose transcript levels differed between control and hCG-treated samples (48 increased, 13 decreased in mean expression level more than 2.5-fold; P < 0.01). Real-time PCR of transcript abundance confirmed up-regulation of several of these, including SerpinA3, matrix metalloproteinase 7, leukemia inhibitory factor (LIF), IL-6, and Complement 3 (P </= 0.05). Analysis of protein abundance in endometrial flushings showed increased LIF and IL-6 protein in uterine flushings from hCG-treated animals compared with controls. Complement C3 and Superoxide dismutase 2 that were also up-regulated, were further evaluated by immunocytochemistry. Complement C3 showed a marked increase in stromal staining in response to hCG, whereas and superoxide dismutase 2 localization was most markedly increased in the glandular epithelial cells. Expression of Soluble Frizzled Related Protein 4, the most highly down-regulated gene, was also validated by PCR. Our experiments have shown that hCG induces alterations in the endometrial expression of genes that regulate embryo attachment, extracellular matrix remodeling and the modulation of the immune response around the implanting blastocyst. Several of these genes, including LIF and gp130, have been shown to be essential for implantation in other species. This study provides strong evidence that the preimplantation embryo itself influences the development of the receptive endometrium via secreted paracrine signals.

Animals↗

PubMed1996

Complement activation and subclassification of tissue immunoglobulin G in the abdominal aortic aneurysm.

Features of autoimmunity in abdominal aortic aneurysm (AAA) have been described, including increases in IgG content. The present experiments were carried out to determine (1) whether the increases in IgG are subclass specific and (2) whether the IgG complex is associated with an increase in the isoforms of complement C3. Seven AAA, four athero-occlusive (AOD), and two normal (NL) aortic tissue extracts were evaluated for immunoreactive complement (C3) components, both by ELISA and by Western immunoblots (probed with a polyclonal goat anti-human C3). The extracts were also assayed for each of the four subclasses of IgG by ELISA (monoclonal mouse anti-human IgGs). Compared to the amounts of IgG by subclass in normal aorta, AAAs had increases of 193-fold in IgG1, 160-fold in IgG2, 389-fold in IgG3, and 627-fold in IgG4. Increases relative to AOD by subclass were smaller, but each subclass was statistically significantly elevated (P < 0.01) over NL or over AOD. There was a 125-fold increase in immunoreactive C3 by ELISA in AAA vs NL, and Western immunoblotting techniques revealed the presence of multiple C3 degradation products. Increases in IgG1, 2, and 3 may be responsible for activation of complement in AAA by the classical pathway. Since the complement system is one of the major effector pathways of inflammation, the presence of complement-fixing IgG subclasses along with increased C3 in the aneurysm wall may be an important mechanism promoting matrix proteolysis in AAA.

Aorta, Abdominal↗

PubMed1983

[The sterile Behçet pustule: a typical skin manifestation of the Behçet syndrome].

Solitary pustules were excised from five patients with Behçet's syndrome and examined histologically, immunohistologically, and--in one case--by immunoelectron microscopy. Histologically the changes were largely confined to the venules of the middle and lower corium. The endothelium was swollen, in part the vascular walls were destroyed. In the perivascular spaces there was round-cell infiltration, mixed with numerous neutrophilic granulocytes, some of them disintegrated. Immunofluorescence-microscopy revealed perivascular deposition of complement C3 and C1q. In fresh lesions there were also IgG or IgM precipitates. Immuno-electron microscopy also demonstrated complement C3 subendothelially. Fibrin deposition and disintegrating neutrophilic granulocytes marked the leukocytoclastic vasculitis. Taken together the findings indicate that an immune-complex vasculitis takes part in the pathogenic mechanism of pustule formation in Behcet's syndrome.

Behcet Syndrome↗

PubMed2003

Lack of a functional alternative complement pathway ameliorates ischemic acute renal failure in mice.

Ischemia/reperfusion (I/R) injury of the kidney is a common cause of acute renal failure (ARF) and is associated with high morbidity and mortality in the intensive care unit. The mechanisms underlying I/R injury are complex. Studies have shown that complement activation contributes to the pathogenesis of I/R injury in the kidney, but the exact mechanisms of complement activation have not been defined. We hypothesized that complement activation in this setting occurs via the alternative pathway and that mice deficient in complement factor B, an essential component of the alternative pathway, would be protected from ischemic ARF. Wild-type mice suffered from a decline in renal function and had significant tubular injury, particularly in the outer medulla, after I/R. We found that factor B-deficient mice (fB(-/-)) developed substantially less functional and morphologic renal injury after I/R. Furthermore, control wild-type mice had an increase in tubulointerstitial complement C3 deposition and neutrophil infiltration in the outer medulla after I/R, whereas fB(-/-) mice demonstrated virtually no C3 deposition or neutrophil infiltration. Our results demonstrate that complement activation in the kidney after I/R occurs exclusively via the alternative pathway, and that selective inhibition of this pathway provides protection to the kidneys from ischemic ARF.

Acute Kidney Injury↗

PubMed1996

Influence of hepatic mitochondrial redox state on complement biosynthesis and activation during and after cardiopulmonary bypass operations.

We have proposed the hazardous phenomena associated with cardiopulmonary bypass (CPB) are due to metabolic derangement by hepatic mitochondrial dysfunction during and after CPB. On the contrary, complement activation and consumption during CPB is reported to be related to the morbidity associated with cardiac surgery. To determine the significance of the hepatic mitochondrial function on the morbidity of cardiac surgery, we measured the serum levels of complements (C3 and C4), activated complements (C3a and C4a), and the arterial ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, in 30 patients undergoing CPB. The AKBR, which was at a normal level preoperatively, dropped to a critical level after the initiation of CPB and remained at a low level during the CPB, returning to the preoperative level on the second postoperative morning in a time dependent fashion. The patients group were assigned to two groups according to their AKBR on the first postoperative morning. Group I consisted of patients whose AKBR had recovered to above 0.7 on the first postoperative morning (n = 16). Group II consisted of the rest of the patients (n = 14). The serum complement concentration had considerably decreased by the end of bypass, but recovered in a time-dependent fashion after CPB. The group I patients (C3: 71% of its preoperative value, C4: 85% of its preoperative value) recovered their complements more quickly than the group II patients (C3: 56% of its preoperative value, C4: 54% of its preoperative value). However, the serum C3a and C4a concentrations increased by the end of bypass (C3a: 806% of its preoperative value, C4a: 341% of its preoperative value). The activated complements were significantly higher in the group II patients (C3a: 124% of its preoperative value, C4a: 236% of its preoperative value) than in the group I patients (C3a: 75% of its preoperative value, C4a: 113% of its preoperative value) on the first postoperative morning. It is suggested that hepatic mitochondrial function is related to recovering the complements and to reducing the activated complements after CPB.

Adolescent↗