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PubMed1983

Hemolytic complement titers and complement C3 levels in endotoxin-induced mastitis.

Escherichia coli lipopolysaccharide B was instilled through the lactiferous duct of cows to induce acute mastitis. Hemolytic complement (C) activity and C3 concentrations were determined in blood serum and in renninprecipitated whey before, and at certain times after, mastitis was induced. Hemolytic complement activity was detected in the whey only during the first 36 hours after endotoxin was instilled, whereas activity was not seen before and 48 or more hours after the endotoxin was given. The maximum titer as measured with the guinea pig RBC/bovine natural antibody system was 1:64. The C3 concentrations in normal whey (before installation of endotoxin), measured by radial immunodiffusion, were between 1% and 4% of the base-line blood serum values (pool from healthy cows). The whey concentration of C3 increased (to 5% to 18%) during the first 8 hours of mastitis. However, at 72 hours, the whey values were back to preinstillation concentrations in all quarters.

Animals↗
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↗
PubMed1989

Analysis of the complement C3 fragments associated with hemodialysis membranes.

During hemodialysis with cuprophan membranes, bioactive peptides are generated because the alternative pathway of complement is activated. When cellulose acetate membranes are employed, complement activation is attenuated. The molecular basis for this improved biocompatibility is unknown. It has been postulated, however, that the complement activating potential of dialysis membranes is influenced by the availability of free hydroxyl groups which would provide an acceptor site for activated C3. To investigate this hypothesis, the forms of C3 associated with cellulose acetate and cuprophan membranes have been analyzed. By Western blot, the predominant form of C3 present on both types of membranes is C3c, a degradation product of C3 that lacks the thiolester necessary for covalent bonding. Minimal amounts of C3d (the region of C3 which contains the thiolester) were observed on both membranes; however, by ELISA, there was no difference in the amount bound to cellulose acetate compared to cuprophan. Further, membrane-associated C3d could be removed by urea, suggesting that it was not bound covalently. These studies indicate that the complement activating potential of dialysis membranes is not determined primarily by the availability of potential covalent binding sites for activated C3b.

Blotting, Western↗
PubMed2006

Complement C3 and C-reactive protein are elevated in South Asians independent of a family history of stroke.

BACKGROUND AND PURPOSE: Complement components are emerging risk factors for cardiovascular disease. In this study, we examined the relation among C3, C-reactive protein (CRP), factor B, and features of the insulin resistance (IR) syndrome in 143 first-degree relatives of South Asian subjects with ischemic stroke, 141 South Asian controls, and 121 white controls. METHODS: C3, CRP (high-sensitivity assay), and factor B levels were measured by ELISAs, and their relation to features of the IR syndrome were assessed. Data are presented as geometric mean (95% CI). RESULTS: There was no significant difference in the levels of C3 between South Asian relatives (1.25 [1.21, 1.29] g/L) and South Asian controls (1.20 [1.15, 1.24] g/L, P=0.2). Levels in both South Asian groups were significantly higher than in white controls (0.95 [0.92, 0.98] g/L; P<0.001 for both comparisons). These differences remained significant after adjustment for covariates. Similarly, levels of CRP were not different between the 2 South Asian groups, but levels in both South Asian groups, after adjustment for covariates, were significantly higher than in white controls. There was no difference in the levels of factor B among the 3 groups. South Asian subjects with elevated C3 levels clustered risk factors associated with IR to a greater extent than those with high CRP. CONCLUSIONS: These results suggest that South Asians have a greater level of chronic subclinical inflammation than do whites, independent of a family history of stroke. In addition, C3 is more likely to cluster with features of the IR syndrome compared with CRP in South Asians.

Adult↗
PubMed1995

Purification and characterization of a human membrane protein that activates the alternative complement pathway and allows the deposition of homologous complement C3.

A human myeloid cell subline, P39+, is found to be a target for human complement (C) via the alternative pathway and to allow the deposition of multiple C3 fragments on its membranes, though expressing the complement regulatory proteins decay-accelerating factor and membrane cofactor protein. The parent cell line, P39-, which is phenotypically similar to the P39+ subline, does not allow the deposition of homologous C3 fragments. In this study, we established a monoclonal antibody, M161 Ab, which reacted with P39+ but not P39- cells. This Ab recognized a 43-kD protein in P39+ cell lysate transblotted onto nitrocellulose. Using this Ab as a probe, we purified the 43-kD protein, namely, M161 antigen (Ag). M161 Ag had a basic isoelectric point (pI), 9.3-9.4 by chromatofocusing, and was precipitated as an insoluble material at the pI point. The purified M161 Ag was a single-chain protein and did not possess N- or O-linked carbohydrates. When the purified M161 Ag was transblotted onto nitrocellulose and incubated with Mg(2+)-EGTA serum, human C3 fragments were efficiently deposited on M161 Ag. The major species of the deposited C3 fragments was C3b. Furthermore, the C3 fragments bound to the M161 Ag were detached by 1 M hydroxylamine, suggesting that a covalent ester linkage sustains M161 Ag-C3b interaction. NH2-terminal amino acid analysis revealed that M161Ag is a novel membrane protein. Hence, it appeared that M161 Ag is a potent activator of human alternative complement pathway on human cells that activates homologous C3 and allows the deposition of C3b on itself. Thus, under some conditions, homeostasis of complement is maintained even on human cells, not only by the complement regulatory proteins, but also by membrane C3-activating molecules on which C3b is deposited.

Antibodies, Monoclonal↗
PubMedDate not supplied

Activation and deposition of human breast-milk complement C3 opsonins on serum sensitive Escherichia coli 0111.

Little is known about the physiological roles and contribution of the human breast-milk complement system in the protection of both the maternal mammary gland and the nursing infant. The ability of a serum-sensitive Escherichia coli to activate the complement components of human breast-milk and colostrum was assessed in vitro. The consequent deposition of C3 fragments, C3b, iC3b and C3dg, on the bacteria was analysed, using a slight modification of a standard ELISA technique for the assessment of activated C3 fragments. The deposition C3 fragments from human milk were demonstrated on the killed bacteria, E. coli NCTC 8007, serotype 0111 K58(B4) H2, using buffers with and without detergent, supporting both the classical and alternative pathways of complement activation. The milk fat appears to competitively inhibit the deposition of these opsonins on the solid-phase bacteria. This study suggests that the complement system is able to contribute to the increased resistance of breast-fed infants against infections.

Breast↗
PubMed2000

Cellular localization of complement C3 and C4 transcripts in intestinal specimens from patients with Crohn's disease.

It has been suggested that the increase in C3 and C4 levels in jejunal perfusates of patients with Crohn's disease (CD) results from local intestinal synthesis of complement. The present study evaluated the expression of these complement genes in inflamed tissues from patients with CD. Surgically resected specimens from patients with CD and control tissue obtained from subjects with adenocarcinoma of the colon were evaluated for C3 and C4 gene expression by the use of 35S-labelled anti-sense RNA probes. All tissue samples, diseased and normal tissue, expressed C4 mRNA throughout in the intestinal epithelium. C3 mRNA was not detected in epithelial cells in histologically normal tissue, but in diseased specimens there was a focal distribution of C3 mRNA in epithelial cells of the crypts, but not in villous epithelium. Focal C3 gene expression correlated with crypt abscess formation and the presence of polymorphonuclear leucocytes in the lumen of the crypts. In addition, C3 mRNA was also found in macrophages of the submucosa. These macrophages were CD68+, fusiform with faint cytoplasm and morphologically different from the large rounded lamina propria macrophages, which do not express C3 mRNA. Multinucleated giant cells did not express either C3 or C4 genes. In addition to its presence in intestinal epithelium, C4 mRNA was also expressed in mast cells, which however did not express C3 mRNA. These observations identify cells in the intestinal wall expressing complement genes and support the hypothesis that there is local regulated production of complement in the intestine of patients with CD, and subsequent complement activation may contribute to the inflammatory process.

Adrenal Cortex Hormones↗
PubMed1990

Glucocorticoid and progestin regulation of eosinophil chemotactic factor and complement C3 in the estrogen-treated rat uterus.

To study the steroid regulation of estradiol-induced uterine eosinophil chemotactic factor activity (ECF-U) in the rat, we injected immature female rats with combinations of estradiol, dexamethasone, progesterone, and the antihormones RU-486 and ketoconazole. An in vitro chemotactic system using blind well chambers and employing eosinophil-differentiated HL-60 promyelocytic cells was used as a bioassay for ECF-U activity. Dexamethasone and progesterone both antagonized the effects of estradiol on stimulation of ECF-U activity; neither hormone induced ECF-U activity when given alone. RU-486 and ketoconazole were able to block the inhibitory effects of dexamethasone and progesterone. The effects of dexamethasone and progesterone appear to be mediated through their specific nuclear receptors and are not due to direct effects on the chemotactic cell. Comparison of the steroid regulation of ECF-U activity with the estradiol-induced synthesis and secretion of complement component C3 showed that progesterone antagonized the effects of estradiol in both systems, whereas dexamethasone was antagonistic on ECF-U, but not on the secretion of C3. Taken together these results suggest that estradiol's effects in the rat uterus may be modulated by other steroids in at least two systems, bringing into question the common practice of studying uterine steroid actions by evaluation of a single protein or mRNA.

Animals↗
PubMed2004

Circulating immune complexes and complement C3 and C4 levels in a selected group of patients with rhinitis in Lebanon.

BACKGROUND: A number of reports indicate that circulating immune complexes (CIC) and activation of the complement system contribute to the pathogenesis of Type I allergy. The aim of this study was to investigate the status of CIC in 113 patients with rhinitis in Lebanon and determine complement components C3 and C4 serum levels in the CIC-positive patients. Serum specific IgE antibodies were previously detected and reported in 74 of the 113 patients. METHODS: CIC were detected by polyethylene glycol precipitation and serum C3 and C4 levels quantified by radial immunodiffusion. RESULTS: CIC was positive in 20 of the specific IgE-positive and 13 of the specific IgE-negative patients. C3 and C4 levels were within the normal range in all the 33 CIC-positive patients. CONCLUSIONS: The antibody class that constitutes the complexes does not seem to be IgG or IgM. Moreover, complement activation does not seem to be involved in the allergic reaction since both C3 and C4 levels were normal in all patients. The role of these complexes, if any, in the pathogenesis of rhinitis is yet to be determined.

Journal Article↗
PubMed1993

Application of the time-resolved immunofluorometric assay to the study of C3 complement component glycation in vitro and in vivo.

A time-resolved immunofluorometric assay (TR-IFMA) was used for the measurement of glycated C3. The very high sensitivity of this technique allowed the direct measurement of glycated and non-glycated proteins (especially C3) in chromatography eluates. C3 glycation in vitro after incubation with 20 mmol/l glucose was always less than 3.5% by day 5. As determined with the TR-IFMA, the means +/- standard deviations of glycated C3 were 0.20% +/- 0.04 for non-diabetic subjects and 0.88% +/- 0.06 for insulin-dependent diabetic patients. The low percentages of glycated C3 in both our in vitro and in vivo studies show that this protein is subject to only moderate rates of glycation.

Adolescent↗
PubMedDate not supplied

Pregnancy-associated plasma protein A (PAPP-A) specifically inhibits the third component of human complement (C3).

Pregnancy-associated plasma protein A (PAPP-A), a macromolecular glycoprotein associated with pregnancy, was shown to inhibit complement-induced haemolysis and to bind heparin reversibly. Because of the inhibitory effects of heparin on the complement cascade it was not clear if the inhibition of complement activity observed with PAPP-A (isolated from heparin plasma) was attributable to the heparin moiety bound to PAPP-A. This work demonstrates that heparin exerts an inhibitory effect on complement activity but that heparin-free PAPP-A is also inhibitory. PAPP-A specifically inhibits C3 by binding to this complement subcomponent and not by inhibiting C3 convertase as demonstrated for C3 inactivator.

Complement C3↗
PubMed1991

Diminished IgG, but not complement C3 or C4 or factor B, precedes nosocomial bacterial sepsis in very low birth weight neonates.

The significance of low serum IgG and complement proteins in very low birth weight (VLBW; less than 1500 g) neonates is not known. Therefore serum IgG, C3, C4 and Factor B were quantitated weekly by rate nephelometry in 15 VLBW neonates who developed proven nosocomial bacterial or candidal sepsis (Group A) and 27 VLBW neonates who did not develop sepsis (Group B). In the first week of life the serum IgG of neonates in Group A was 295 +/- 33 mg/dl (mean +/- SEM) and in Group B it was 440 +/- 21 mg/dl (P less than 0.01). In the second week, the IgG of Group A was 270 +/- 32 mg/dl and that of Group B was 473 +/- 38 mg/dl (P less than 0.01). If the IgG was less than 350 mg/dl in the first week or less than 230 mg/dl in the second week, the relative risk of acquiring sepsis was greater than or equal to 5 (95% confidence interval in the first week, 1.7 to 11.2). The serum IgG was measured before the onset of sepsis in 14 of the 15 neonates in Group A. In the week before sepsis the IgG of the 14 neonates was less than 440 mg/dl (range, 45 to 433 mg/dl) in all cases, was below the mean IgG of Group B in 12 of 14 cases (P = 0.006 vs. Group B) and was greater than 2 SD below the mean IgG of Group B in 4 of 14 cases (P = 0.0003 vs. Group B).(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Infections↗