C3 complement components & their breakdown product (C3d) in patients of thromboangiitis obliterans.
Explore the source record for details and available documents.
Adult↗
SEARCH · Search PubMed
Results for “Complement C3”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Serum immunoglobulins and C3 complement concentrations in malignancy.
Explore the source record for details and available documents.
Aged↗
Changes in complement C3 levels following treatment of patients with Brugia malayi infection.
Serum IgG levels and complement C3 levels were assayed on Day 0, 1, 3-4, 7 and 56-70 post-treatment with diethylcarbamizine citrate (DEC) in a series to 26 patients with Brugia malayi infection and 6 volunteers without infection. On treatment, the microfilariae were cleared from the blood within 24 hours. The eosinophils decreased dramatically on Day 1 post-treatment but increased rapidly by Day 4 to 7 and then dropped to normal levels in 45 days. The serum IgG mean levels decreased briefly following treatment with DEC but then returned to original levels. However, the complement C3 levels gradually increased over the 2 months period of study reaching statistical significance levels (p less than 0.01) in patients with initial high blood microfilariae. The observation suggests that Brugia malayi infection probably induces a high rate of synthesis of complement C3 and this process continued in the post-treatment phase. Since, DEC treatment did not cause a decrease in complement C3 with the elimination of blood microfilariae, it would appear that the complement C3 is consumed following antibody attachment to the microfilariae as they enter the blood circulation.
Adult↗
C3 complement types in northern Greece.
The C3 complement types were studied in 463 patients with thyroid diseases and in 211 controls. There were no significant differences with respect to gene or phenotype frequencies between patient groups and controls. In the total sample, the gene frequencies are similar to those found in other European populations.
Adult↗
Immunofluorescent studies of complement C3 in the hair follicles of normal scalp and of scalp affected by alopecia areata.
The deposition of complement C3 in the hair follicles of scalps of 4 normal subjects and of the affected parts of 9 patients with alopecia areata was found by the direct immunofluorescent methods. No deposition of immunoglobulins (IgG, IgA, IgM, IgD and IgE) was found. In the normal scalps, complement C3 was found to be deposited in the hyaline membrane of the hair bulb and in the internal layer of connective tissue sheath at the lower about 2/3 transient portion of anagen follicles, and in the thickened hyaline membrane of the catagen follicles. The deposition of complement C3 was also found in the anagen and catagen-like hair follicles even in the patients with alopecia areata, which was similar to the finding in the normal scalps. From the fact that the deposition of complement C3 was found chiefly in the transient portion of the hair follicles of the normal scalps, and that the behavior of deposition of complement C3 reflected the morphological state of hair follicles in each stage of the hair cycle, even in alopecia areata, complement C3 may be intimately related to the hair cycle, even though its significance is as yet unknown.
Adult↗
Administration of a soluble recombinant complement C3 inhibitor protects against renal disease in MRL/lpr mice.
Complement receptor 1-related gene/protein y (Crry) in rodents is a potent membrane complement regulator that inhibits complement C3 activation by both classical and alternative pathways. To clarify the role of complement in lupus nephritis, MRL/lpr mice were given Crry as a recombinant protein (Crry-Ig) from 12 to 24 wk of age. Control groups were given saline or normal mouse IgG. Sera and urine were collected biweekly. Only 1 of 20 (5%) Crry-Ig-treated mice developed renal failure (BUN > 50 mg/dl) compared with 18 of 38 (47.4%) mice in control groups (P = 0.001). BUN levels at 24 wk were reduced from 68.8 +/- 9.7 mg/dl in control groups to 38.5 +/- 3.9 mg/dl in the Crry-Ig-treated group (P < 0.01). Urinary albumin excretion at 24 wk was also significantly reduced from 5.3 +/- 1.4 mg/mg creatinine in the control groups to 0.5 +/- 0.2 mg/mg creatinine in the Crry-Ig-treated group (P < 0.05). Of the histologic data at 24 wk, there was a significant reduction in scores for glomerulosclerosis and C3d, IgG, IgG3, and IgA staining intensity in glomeruli in complement-inhibited animals. Crry-Ig-treated animals were also protected from vasculitic lesions. Although there was no effect on relevant autoimmune manifestations such as anti-double stranded DNA titers or cryoglobulin IgG3 levels, circulating immune complex levels were markedly higher in complement-inhibited animals. Thus, inhibition of complement activation with Crry-Ig significantly reduces renal disease in MRL/lpr lupus mice. The data support the strategy of using recombinant complement C3 inhibitors to treat human lupus nephritis.
Albuminuria↗
[Decrease in the serum level of the C3 complement component in noninsulin dependent diabetes of recent onset].
Complement components C3, C4 and C3A were measured by immuno-diffusion in plasma of 36 recent onset insulin-dependent diabetics (IDD) and compared to plasma complement levels of 19 long-standing IDD and 18 non diabetic controls. A significant decrease of C3 and a mild increase of C3A was found in recent-onset diabetes group. However these variations could not be correlated with IgG-islet cell antibodies, C3--fixing islet cell antibodies or A--B HLA antigens. No significant difference was found between long-standing IDD and controls for the 3 complement components. In conclusion, the decrease of C3, found in 30% of recent onset IDD, might be due to increase complement consumption either by the insulitis process or by circulating immune complexes.
Adolescent↗
Levels of complement C3 and C4 components in Amerindians living in an area with high prevalence of tuberculosis.
The levels of complement C3 and C4 components were determined in non-indigenous (creoles) and indigenous (Warao) populations, the latter with an extremely high tuberculosis (TB) rate. Serum samples from 209 adults were studied and classified in 4 groups taking into account tuberculin skin tests (TST): (1) the group of Warao patients (58 positive for the TST, WP TST+ and 9 negative for the TST, WP TST-), (2) the group of creole patients (34 positive for the TST, CP TST+ and 9 negative for the TST, CP TST-), (3) the group of healthy Warao controls (38 positive and 14 negative for TST, WC TST+ and WC TST-, respectively), (4) the creole controls (26 positive and 21 negative for the TST, CC TST+ and CC TST-, respectively). With respect to the results concerning the measurement of both complement C3 and C4 components with the exception of the WC TST and the CC groups, the WP TST+ and WP TST- as well as WC TST+ groups showed a significant frequency of individuals with decreased levels of complement C3 component (20.6, 33.3, and 26.3%, respectively) and also C4 component (12.0, 11.1, and 13.3%, respectively) in comparison to both creole patients (CP TST+, 8.82% and CP TST-, 0% and CP TST+, 5.88% and CP TST-, 0%) for C3 and C4, respectively. The study of these parameters carried out in 15 Warao subjects with active infection, before and after anti-TB chemotherapy,statisticallyconfirmedthat the effective chemotherapy did not restore normal levels of the complement C3 and C4 components among Warao patients. Aditional tests for hepatitis B or hepatitis C infection, and the profile of the hepatic proteins were not associated to the deficiency in production of the complement components. In conclusion, the results show that within the Warao population, a high percentage of subjects exhibit decreased levels of both complement C3 and C4 components independent of latent or active infection and the status of TST.
Adolescent↗
The effect of cigarette smoking on ceruloplasmin and C3 complement: risk of cardiovascular disease (atherosclerosis).
Serum ceruloplasmin, C3 complement and albumin in 119 male smokers and 65 male non-smoker; from a military unit in Bangkok were investigated in this study. The serum ceruloplasmin concentration was found to be significantly higher in smokers than in non-smokers. However, the serum albumin concentration in smokers was statistically significantly lower than in non-smokers. Significant associations were also found between ages, albumin levels and the quantity of cigarettes smoked. There was a significant positive correlation between serum ceruloplasmin and C3 complement concentrations. An association between the quantity of cigarettes smoked and albumin was also found, as well as a significant relationship between smoking and the quantities of cigarettes smoked to serum ceruloplasmin levels when smoking and the quantity of cigarettes smoked were taken as independent variables, and the serum ceruloplasmin levels as a dependent variable. This might suggest that high concentrations of the acute-phase protein, i.e. ceruloplasmin, might constitute a risk of developing atherosclerosis or cardiovascular disease in smokers.
Adult↗
Covalent attachment of human complement C3 to IgG. Identification of the amino acid residue involved in ester linkage formation.
C3 (native complement component 3) plays a central role in the activation of complement and in the transport and processing of immune complexes. Proteolytic activation of C3 exposes a highly reactive thioester bond which preferentially reacts with the hydroxyl groups of acceptor molecules on activators such as immune complexes or carbohydrates on microorganisms. Recently, a C3 attachment site has been localized on the CH1 domain of IgG1 between Val134 and Lys156. We have synthesized a series of peptide analogs of this region to identify the preferred residue for C3b (the proteolytically activated form of C3) attachment. The parent peptide included all 6 hydroxyl-containing amino acids present in the proposed binding site and was highly reactive with activated C3. The C3b-peptide complex was sensitive to hydroxylamine as was C3b-IgG indicating that both were ester-linked. The kinetic profile of hydrolysis of the C3b-peptide complex under physiologic conditions was found to be nearly identical to the profiles of C3b-IgG, C3b-IgG1, and C3b-glycerol complexes. Site-specific amino acid substitution of threonine and serine residues in the peptide indicated that, in contrast to the attachment site in C4b, little or no attachment occurred at serine residues. The threonine corresponding to Thr144 in the CH1 domain of IgG was found to be the major acceptor site for C3b. Thr148 was the second most reactive site on the peptide, but this residue is buried in native IgG.
Amino Acid Sequence↗
Synthesis and regulation of the fourth component of complement (C4) in the human monocytic cell line U937: comparison with that of the third component of complement (C3).
Production of the fourth component of complement (C4) by the human monocytic cell line U937 and its regulation were investigated in comparison with the production of the third component of complement (C3) in a cell culture system. Although no detectable C4 was produced by U937 without stimulation, U937 was induced by recombinant interferon-gamma (IFN-gamma) to synthesize C4 in a dose- and time-dependent fashion. The production of C4 was reversibly inhibited by cycloheximide, indicating that it resulted from de novo synthesis. The C4 synthesized by U937 cells was functionally active as assessed by haemolytic assay. SDS-PAGE following biosynthetic labelling showed that subunit structure of C4 synthesized by U937 cells was identical with that of plasma C4 but that molecular weight of alpha-chain was greater than that of plasma C4. We compared the regulation of C4 synthesis with that of C3 synthesis. Although C3 synthesis by U937 cells was enhanced by IFN-gamma, lipopolysaccharide (LPS) and phorbol myristate acetate (PMA), C4 synthesis was induced only by IFN-gamma. LPS and IFN-gamma induced a synergistic increase in C3 synthesis by U937 cells. U937 cells incubated with LPS and IFN-gamma synthesized a greater amount of C4 than those incubated with IFN-gamma alone. Thus it was demonstrated that the synthesis of C3 and C4 was independently regulated. This study shows that the U937 cell line provides a useful model for studies on the synthesis of complement proteins and on the regulation of complement production.
Cell Line↗
Phylogeny of the third component of complement, C3: analysis of the conservation of human CR1, CR2, H, and B binding sites, concanavalin A binding sites, and thiolester bond in the C3 from different species.
The third component of complement, C3, binds to several other complement proteins. To study the diverse reactivities of C3, we analyzed the conservation of structural and functional features in the C3 from different species. First, we developed a method to purify swine (Po), rabbit (Rb), mouse (Mo), cobra (Co), Xenopus (Xe), axolotl (Ax), and trout (Tr) C3 from plasma. This involved protein precipitation by polyethylene glycol, followed by anion-exchange, gel filtration, and cation exchange chromatography. All C3's tested were comprised of two chains (alpha/beta-chain) and contain a thiolester bond within the alpha-chain. The two N-linked high-mannose carbohydrates found in human C3 were only conserved (as detected by ConA binding) in Rb C3. In contrast, Xe, Ax, and Tr C3 have this moiety only in the beta-chain and Po and Mo C3 only in the alpha-chain. Co C3, in contrast to cobra venom factor (CVF), lacks ConA binding carbohydrates in both chains. N-terminal amino acid sequence analysis of the alpha-, alpha'-, and beta-chains showed varying degrees of similarity within the different C3's. The N-termini of the Xe and Ax C3 beta-chains were found to be blocked. The conservation of binding sites in the different C3's for human complement receptors type one (CR1) and two (CR2) and for factors H and B was investigated due to the structural and functional similarities of these molecules and to the ability of some of them to bind to the same domain(s) in human C3.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Sequence↗
Analysis of inflammatory cells and complement C3 in bupivacaine-induced myonecrosis.
Immunohistochemical analysis of the inflammatory cells and complement C3 in the rat skeletal muscle was performed chronologically in bupivacaine-induced myonecrosis. At 30 minutes after injection, polymorphonuclear leukocytes appeared and increased in number, with a peak value at 12 hours, while macrophages reached the highest level at 2 days. In contrast, T cells comprised only a small population. Two weeks after the injection, all types of the inflammatory cells returned to the normal level. Deposition of complement C3 was recognized at 60 minutes at the surface membrane of degenerating muscle fiber. Our observation suggests the importance of both polymorphonuclear leukocytes and complement C3 in the early stage, and macrophages in the later stage of bupivacaine-induced myonecrosis. In addition, our findings cast doubt on the pathological significance of T cells in this model.
Animals↗
[The relationship between complement C3 receptors (CR1, CR3) on polymorphonuclear leukocytes and complement fragments during hemodialysis].
The expression of complement receptor type 1 (CR1) and type 3 (CR3) on polymorphonuclear leukocytes (PMNs) and generation of complement fragments, C3a, C5a, C4d, iC3b and Bb, were studied in patients during hemodialysis using cuprammonium rayon (Cu) membranes. Furthermore, the relation between the expression of CR1 and CR3 on PMNs from healthy donors and complement fragments was investigated. The expression of CR1 and CR3 on PMNs increased during hemodialysis. Plasma C3a, C5a and iC3b levels increased in the first 15 minutes and then decreased at 120 minutes of dialysis. But plasma Bb level remained high until the end of hemodialysis. Purified Bb had no effect on the expression of CR1 and CR3 on PMNs, but C5a augmented those expression in vitro. Nafamostat mesilate, an artificial proteinase inhibitor, inhibited augmentation of complement receptors on PMNs in concentration dependent fashion. C5a generated through the activation of complement was thought to take an important role in the increased expression of CR1 and CR3 on PMNs.
Aged↗
Activation of the endothelium by IL-1 alpha and glucocorticoids results in major increase of complement C3 and factor B production and generation of C3a.
Constitutive secretion of complement C3 and factor B by the endothelial cell (EC) is lowered by therapeutic concentrations of glucocorticoids such as hydrocortisone or dexamethasone, whereas regulatory protein factor H production is increased by these hormones. In contrast, the proinflammatory cytokine IL-1 alpha has a stimulatory effect on C3 and factor B secretion by the endothelium and an inhibitory effect on factor H secretion. In this study, we examined the combined effect of IL-1 alpha and glucocorticoids on C3 and factor B expression by the endothelial cell. When dexamethasone or hydrocortisone were added to IL-1 alpha, significant potentialization of IL-1 alpha-induced stimulation of C3 and factor B production was observed, occurring at various concentrations of either stimuli. Dose-response experiments indicate that, in vitro, optimal concentrations are in the range of 10(-7) to 10(-5) M for dexamethasone and 50-200 U for IL-1 alpha. In contrast, dexamethasone counteracts, in an additive way, the inhibitory effect of IL-1 alpha on regulatory complement protein factor H production by EC. Such a potentialization between glucocorticoids and IL-1 alpha was not observed for another marker of endothelial activation, IL-1 alpha-induced stimulation of coagulation tissue factor expression. The association of glucocorticoids and IL-1 alpha therefore appears to be a specific and major stimulus for the secretion of complement C3 and factor B, two acute-phase proteins, by the endothelium. As a result of the in vitro endothelium stimulation by glucocorticoids and IL-1 alpha, C3a is generated in the vicinity of the endothelial cell. This study further suggests that complement activation, with its deleterious consequences, may result from the stimulation of endothelium in situations where high levels of IL-1 alpha and endogenous glucocorticoids coexist, such as in septic shock.
Cells, Cultured↗
Heat-induced thiol-disulfide interchange reaction on the third component of human complement, C3.
The third component of human complement, C3 is composed of two disulfide-bridged polypeptide chains of Mr 120,000 (alpha chain) and Mr 70,000 (beta chain). C3 has a thioester bond that serves as a binding site for targets when C3 is activated. Heat treatment of C3 induces autolytic peptide bond cleavage at the thioester site in the alpha chain as well as rupture of the thioester bond. The alpha chain fragments are linked to each other and beta chain via disulfide bonds. This study, however, documented that prolonged heating gave rise to liberation of several fragments including beta and the larger fragment of alpha chain. Using a fluorescent thiol reagent and [14C]iodoacetamide, we analyzed thiol residues present on each fragment, and elucidated that the thiol residue exposed by rupture of the thioester bond shifts in turn to another fragment resulting in the liberation of the fragments. The results were compatible with those on C4, and suggested that the generated thiol residue induces thiol-disulfide interchange reaction. On heating of plasma, fragments of C3 were not released, while the cleavage of the alpha chain occurred more effectively. The heated C3 (56 degrees C, 15 min) became insusceptible to C3b inactivator (I) and factor H, suggesting that additional conformational change is accompanied with cleavage of the thioester bond.
Complement C3↗
Bf and C3 complement types in rheumatoid arthritis.
Bf and C3 complement types were studied in 100 male and 100 females patients from northern Sweden with erosive rheumatoid arthritis (RA) and compared with population controls. A significantly decreased frequency of the Bf FS phenotype was found particularly in males and in patients with a family history of polyarthritis. Significant Bf associations were also found with a more severe form of RA (functional classes III and IV) and with high titers of the rheumatoid factor. No significant difference with respect to C3 phenotype and gene frequencies was found between RA patients and controls. Thus, the association between RA and C3F found in some previous investigations was not confirmed.
Arthritis, Rheumatoid↗
Binding of complement C3 to Klebsiella pneumoniae treated with sub-MIC cefodizime and chemiluminescence response of human polymorphonuclear leukocytes.
The binding of complement C3 to the cell surface of Klebsiella pneumoniae exposed to human serum complement after treatment with or without sub-MIC of antibiotics was examined by double diffusion immunoprecipitation against anti-human complement C3, and the production of oxygen-derived radicals by human polymorphonuclear leukocytes stimulated by complement-opsonized K. pneumoniae after treatment with or without sub-MIC of antibiotics was measured using the chemiluminescence (CL) assay. Complement C3 bound to the cell surface of K. pneumoniae treated with cefodizime was detected after exposure to human serum complement. The CL response induced by complement-opsonized bacteria after treatment with cefodizime was much higher than the response induced by nontreated bacteria or complement-opsonized bacteria after treatment with other antibiotics. These findings indicate that treatment with sub-MIC cefodizime make K. pneumoniae more susceptible to opsonization by complement and promotes the specific phagocytosis mediated by complement receptors.
Cefotaxime↗