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PubMed1994

Serum complement levels in asymptomatic Plasmodium falciparum parasitaemic children.

Twenty-eight (42%) of 67 afebrile children (mean age 6.3 +/- 3.6 years) undergoing various minor elective surgeries were slide positive for malaria parasitaemia. All infected subjects were given oral chloroquine therapy before and after blood samples were collected. Pre- and post-treatment complement (C4, C3, Bf and CH50 levels were evaluated in 15 of the subjects who had parasite densities > or = 500/microliter. These were compared with the levels in 15 age/sex-matched children who had acute malaria, as well as with the levels in 15 age/sex matched, non-infected controls. Significant consumption of C4 was observed in both the asymptomatic (p < 0.05) and symptomatic (p < 0.05) subjects. The mean serum levels of C4 were significantly higher in the asymptomatic, when compared with the symptomatic subjects (p < 0.01), and the healthy controls (p < 0.05). The distribution of classical pathway complement haemolytic titres in the groups studied was the same as that of the C4 levels. It is concluded that the forth component of the classical complement pathway may play a protective role in asymptomatic malaria.

Child↗
PubMed1978

Alternate pathway activation of complement in a Proteus mirabilis ulceration of the cornea.

A 63-year-old patient had an extensive infiltration, ulceration, and eventual perforation of the cornea caused by Proteus mirabilis. Histopathological examination of corneal tissue that was obtained at keratoplasty disclosed that the stroma was ulcerated with a diffuse infiltration of polymorphonuclear leukocytes. Immunopathological examination of the cornea revealed prominent and diffuse staining for properdin and C3 complement. There was an absence of staining for IgG, IgA, IgM, IgE, and C4 complement. These findings suggest that the alternate pathway of complement was activated in this ulcerated cornea and that immunopathological phenomena contribute to the polymorphonuclear infiltration found with Gram-negative ulcerations of the human cornea.

Complement C3↗
PubMed2001

Induction of the complement component C1qB in brain of transgenic mice with neuronal overexpression of human cyclooxygenase-2.

We report that overexpression of human (h) cyclooxygenase-2 h(COX-2) in the brain of a transgenic mouse line leads to selective induction of endogenous complement component C1qB expression in neurons. No detectable induction of the C3 and C4 complement components in the brain was found. Chronic treatment of mice with the selective COX-2 inhibitor nimesulide reduced the hCOX-2-mediated induction of hippocampal C1qB mRNA expression. The data suggest that neuronal COX-2 expression may influence inflammatory responses in the brain, in part through modulation of complement gene expression. Because there is extensive evidence that C1q and other complement components are involved in Alzheimer's disease (AD) neurodegeneration, this study advances our understanding of the apparent benefits of COX-2 inhibition in AD.

Alzheimer Disease↗
PubMed2000

Molecular cloning and linkage analysis of complement C3 and C4 genes of the Japanese medaka fish.

The thioester-containing complement components, C3 and C4, are believed to have arisen by gene duplication from a common ancestor, and the mammalian C4 gene resides in the vicinity of the C2 and B genes within the major histocompatibility complex (MHC) class III region. To analyze the evolution of both the complement system and the MHC, we determined the complete primary structures of two C3 genes, termed Orla C3-1 and Orla C3-2, and one C4 gene, termed Orla C4, of a teleost, Japanese medaka fish (Oryzias latipes), by analyzing cDNA clones isolated from a liver library constructed using the inbred AA2 strain. The deduced basic structures of Orla C3-1, C3-2, and C4, such as the subunit chain structure, the thioester site, and the proteolytic activation site, are similar to their mammalian counterparts. However, the catalytic His residue which greatly increases the rate of thioester reaction, is replaced by Ala in Orla C3-2, implying functional differentiation between two C3 molecules. Mapping analysis revealed a close linkage between the C3-1 and C3-2 genes, indicating that they arose by a local duplication rather than by a genome-wide tetraploidization. The C4 gene belongs to a different linkage group, and no linkage was observed among the C3, C4, Bf/C2, MHC class I, and MHC class II loci. These results suggest that the MHC class III complement region was established in the tetrapod lineage, or lost in the teleost lineage.

Amino Acid Sequence↗
PubMedDate not supplied

Complement C2, C3, C4 and factor B allele distribution in the Gipsy population in Hungary.

Allotype frequencies of four complement proteins (C3, C2, factor B, and C4) were tested in 150 healthy Hungarian and 126 healthy Gipsy individuals living in Hungary. We observed significant differences between the two ethnic groups in the incidence of C3*F, Bf*F, C4A*Q0, C4A*3, C4B*1 and C4B*2 allotypes. Bf*F occurred more frequently among Gipsies, while frequencies for the other three allotypes was lower in this group than in Hungarians. The similarities in the allotype frequencies of C3 and Bf among Gipsy and Gaddis (India) populations supports the Indian origin of the former ethnic group.

Adult↗
PubMed1990

[A comparative study of serum complement (C3 and C4) in inflammatory joint diseases].

The third and the fourth fraction of the complement (C3 and C4), haptoglobin, fibrinogen, alpha 1-glycoprotein, alpha 2-macroglobulin and transferrin were examined in 692 patients with inflammatory joint disease--rheumatism, rheumatoid arthritis, ankylosing spondylarthritis, psoriatic arthritis, Reiter's syndrome, sacroiliitis [correction of sacroileitis], reactive arthritis, gout, osteoarthrosis and nosologically undefined arthritis in active or nonactive phase and in 60 healthy controls. The complement fractions studied show an increase of various degree and importance in almost all groups of patients in both phases studied. The relations between the complement fractions and the other acute phase indices show significant correlations between them and the other acute phase indices. C3 and to a certain degree C4 could be added to the acute phase reacting indices. Their place in the downgrade scale is as follows: fibrinogen, haptoglobin, alpha 1-glycoprotein, C3, C4, alpha 2-macroglobulin, transferrin.

Acute-Phase Proteins↗
PubMed1986

Detection of disulphide bonds and localization of interchain linkages in the third (C3) and the fourth (C4) components of human complement.

Disulphide bonds contribute significantly to the maintenance of structural/functional integrity of many proteins. Therefore it was of interest to study the distribution and the effect of disulphides on conformation of complement components C3 and C4. These proteins are precursors of several fragments with various binding sites and distinct physiological functions. The constituents of C3c (beta, alpha 27, alpha 43) and those of C4c (beta, alpha 27, alpha 16, gamma) were investigated, since other fragments of C3 or C4 do not participate in interchain linkages. Inter-and intra-chain disulphide bonds in C3c and C4c were localized by using a modification of conventional SDS (sodium dodecyl sulphate)/polyacrylamide-gel electrophoresis such that the change in mobility of disulphide-bond-containing proteins can be detected throughout the transition from a non-reduced to a fully reduced state. Several forms of the alpha 43 fragment from C3, and of the gamma-chain of C4, with different mobilities can exist, depending on the number of intra-chain disulphide bonds reduced. The intermediates (heterodimers) generated by a partial reduction of C3c or C4c were characterized by two-dimensional SDS/polyacrylamide-gel electrophoresis performed in the absence, then in the presence, of beta-mercaptoethanol. The inter-chain linkages in C3c were determined to be beta-alpha 27 and alpha 27- alpha 43, thus indicating the presence of only one interchain bond in C3. The two interchain bonds in C4c are beta-alpha 27 and alpha 16-gamma. The third interchain bond in C4 (alpha 27-gamma, tentative) remains to be determined.

Complement C3↗
PubMed1983

Partial genetic deficiency of the C4 component of complement in discoid lupus erythematosus and urticaria/angioedema.

A high incidence of discoid lupus erythematosus (DLE) and urticaria/angioedema was found among patients with selective low levels of the C4 component of complement. Although evidence for activation of C4 was present in patients' sera, studies to determine the presence of known activation mechanisms were negative. Genetic C4 typing in four pedigrees showed that all propositi carried the null allele B*QO. It is postulated that the low C4 levels in these patients are related to the skin lesions and this partial genetic deficiency.

Adult↗
PubMed1985

The determination of the complement components C1q, C4 and C3 in serum and cerebrospinal fluid by radioimmunoassay.

Non-competitive 2-site radioimmunoassays (RIA) for the determination of the complement proteins C1q, C4 and C3 in cerebrospinal fluid (CSF) are described. The quantitative results of the RIAs were the same as those obtained by other assay methods: radial immunodiffusion and turbidimetry and, in the case of C4, the haemolytic assay. The concentrations of the complement proteins in paired CSF and serum samples from a group of 60 patients were measured, as well as those of albumin and IgG. The ratios (concentration in CSF)/(concentration in serum) of the complement proteins correlated poorly with that of albumin. In contrast, the ratio of IgG was significantly correlated with that of albumin. The ratios of the complement proteins were higher than might be expected on the basis of their molecular masses. This suggests that these proteins may be synthesized within the normal central nervous system.

Adolescent↗
PubMed1982

Comparison of a fluorometric method with radial immunodiffusion assays for determination of complement components C3 and C4.

Measurements of patient serum complement components C3 and C4 are useful indicators of complement consumption in immune complex diseases. A fluorometric quantitative immunofluorescence system was evaluated in terms of measuring these complement components, and the results were compared with those of radial immunodiffusion assays. For comparison of the two systems, 232 patient sera were evaluated for C3, and 202 specimens were tested for C4. Analysis of the data by linear regression indicated a proportional difference between the methods. C3 and C4 concentrations measured by the fluorometric method were lower than those measured by radial immunodiffusion, especially concentrations exceeding the normal ranges. In detecting lower concentrations (less than 120 mg/dl for C3 and less than 25 mg/dl for C4), the two methods showed better agreement. Each assay system was reproducible and could be used to evaluate changes that occur in concentrations of complement components during therapeutic treatment. However, the ease in processing a large volume of specimens and the short time needed to complete the assay are advantages that make the fluorometric method more suitable than radial immunodiffusion for use in a large clinical laboratory.

Complement C3↗
PubMed1981

Interaction between the labile binding site of human C4 and methylamine.

Human complement component C4 was irreversibly inactivated by low concentrations of methylamine at slightly alkaline pH. The inactivated C4 molecules lost the ability to bind to EAC1 cells but retained th capacity to participate in the formation of classical pathway C3 convertase in the fluid phase. 14C-methylamine was incorporated into the alpha-chain at a ratio of 1 mol methylamine per mol C4.

Complement C4↗
PubMed1976

Mode of interaction of different polyanions with the first (C1,C1) the second (C2) and the fourth (C4) component of complement. IV. Activation of C1 in serum by polyanions.

Treatment of serum with dextransulphate polyvinylsulphate or polyanetholsulphonate resulted in a dose-dependent activation of C1 and C3; this was found for normal serum as well as for C4-deficient guinea-pig serum. Activation of C1 and C3 occurred at the same concentration of polyanions. The consumption of C3 in C4 deficient serum and the requirement of factor D of the alternative pathway indicate that C3 is activated via the alternative pathway.

Animals↗
PubMed1986

Studies of HLA, factor B (Bf), complement C2 and C4 haplotypes in type 1 diabetic and control families from northern Sweden.

The HLA-A,-B,-C,-DR antigens and the complement factors C2, C4 and Bf were determined in 30 insulin-dependent diabetes mellitus (IDDM) patients and 30 healthy controls from northern Sweden. Family studies allowed the deduction of extended haplotypes in the HLA and complement systems. Phenotype studies revealed significant associations between IDDM and HLA-DR4 (p less than 0.001), HLA-DR3 (p less than 0.05), HLA-DR3/4 (p less than 0.025), C4-B3 (p less than 0.001) and Bf-S (p less than 0.025). Haplotype studies showed that the extended haplotype [HLA-B15, C2-1, C4-A3B3, Bf-S, HLA-DR4] had a particularly strong association to IDDM. This haplotype was found in 10 out of 30 IDDM probands but in none of 30 control children and accounts for practically all the C4-B3 allotypes among the 30 IDDM probands. The C4-B3 gene therefore seems to be a valuable marker for IDDM. No haplotype containing HLA-DR3 was increased in frequency among the IDDM probands. The extended haplotype [HLA-B7, C2-1, C4-A3B1, Bf-S, HLA-DR2] present among the controls was absent in the IDDM probands. The frequency of the extended haplotype [HLA-B15, C2-1, C4-A3B3, Bf-S, HLA-DR4] was increased also among the parents to the IDDM probands compared to those of the control parents, whereas the frequency of [HLA-B7, C2-1, C4-A3B1, Bf-S, HLA-DR2] was decreased. The extended haplotype [HLA-B8, C2-1, C4-B1, Bf-S, HLA-DR3] was more common among the males (p less than 0.05) compared to the females in the total material. The family analysis showed that 3 out of 5 affected sibs shared both haplotypes with their IDDM proband. This was the case for only 3 out of 35 unaffected sibs.

Adolescent↗
PubMed1983

Effect of maternal nutritional status on immunological substances in human colostrum and milk.

Substances in colostrum and breast milk confer significant disease resistance to the breast-fed infant. The influence of maternal nutritional status on both immunological and nonimmunological milk factors was studied in a group of 23 Colombian women during the first 2 months of lactation. Maternal malnutrition was characterized by significantly lower weight/height ratio, creatinine/height index, total serum proteins, serum albumin, and serum IgG and IgA. The colostrum of malnourished mothers contained only one-third the normal concentration of immunoglobulin G and less than half the normal level of albumin. Significant reductions in colostrum levels of IgA and the fourth component of complement (C4) were also observed in the malnourished group. No differences were observed in colostral concentrations of lysozyme, C3 complement, or IgM. Titers of antibody in milk directed against respiratory syncytial virus were not influenced by maternal nutritional status. The differences noted above tended to disappear in mature milk, concomitant with improvement in the nutritional status of malnourished mothers during the first several weeks postpartum. We conclude that the protective qualities of colostrum and milk may be significantly influenced by maternal nutritional status.

Adult↗
PubMed1997

Complement activation by heparin-protamine complexes during cardiopulmonary bypass: effect of C4A null allele.

OBJECTIVES: The first objective was to determine the effect of inherited differences in the classic pathway complement protein C4 on complement activation by heparin-protamine complexes in cardiac surgery. Specifically, we hypothesized that patients with heterozygous C4A null phenotype (A0BB), who have decreased amounts of C4A, may have increased complement activation because of reduced clearance of heparin-protamine complexes. The second objective was to determine whether heparin-protamine-induced complement activation correlated with postoperative pulmonary shunt fractions. METHODS: C4 typing was performed by agarose gel immunofixation and crossed immunoelectrophoresis. Complement activation was measured by radioimmunoassay of C3a and C4a before cardiopulmonary bypass, after bypass, and after protamine infusion. Shunt fractions were calculated from blood gases. RESULTS: Of the 79 patients, 18 expressed heterozygous C4A null allele (A0BB), 16 had heterozygous C4B null allele (AAB0), three had homozygous C4B null alleles (AA00), and the rest expressed both C4A and C4B alleles (AABB). Patients with heterozygous C4A null allele had significantly increased plasma levels of C4a after protamine neutralization of heparin (C4a of 2862 +/- 375 ng/ml; mean +/- standard error of the mean) when compared with patients with normal expression of C4 alleles (AABB) (C4a of 1580 +/- 141 ng/ml) or heterozygous C4B null allele (C4a 1526 +/- 208 ng/ml). Pulmonary shunt fractions obtained after the operation correlated with the classic pathway complement activation by heparin-protamine complexes, but not with alternative pathway complement activation during cardiopulmonary bypass. CONCLUSIONS: Patients with heterozygous C4A null phenotype have increased complement activation by heparin-protamine complexes during cardiac operations, possibly because of their defective clearance. The classic pathway complement activation by heparin-protamine interaction correlates with postoperative pulmonary shunt fractions.

Alleles↗
PubMed2006

Pivotal role of complement-fixing HLA alloantibodies in presensitized kidney allograft recipients.

Recipient presensitization represents a major risk factor for kidney allograft loss. Complement fixation may be a critical attribute of deleterious alloantibodies. We investigated clinical impact of complement-fixing HLA presensitization employing [C4d]FlowPRA, a novel assay permitting selective detection of HLA panel reactive antibody (PRA)-triggered C4 complement split product deposition. A cohort of 338 kidney transplants was evaluated for presensitization applying [C4d]FlowPRA together with [IgG]FlowPRA and complement-dependent cytotoxicity (CDC)-PRA. Analysis of HLA class I alloreactivities revealed a high incidence of C4d-positive graft dysfunction in [IgG]FlowPRA(+)/[C4d]FlowPRA(+) and [IgG]FlowPRA(+)/[C4d]FlowPRA(-) recipients (23% and 22% vs. 3% in [IgG]FlowPRA(-) patients). Only patients with complement-fixing HLA class I immunization had inferior graft survival [75% (3 years) vs. 91% and 89%, respectively (p=0.036)]. Despite frequent finding of capillary C4d deposition (28%), complement-fixing HLA class II immunization was not associated with inferior survival rates. This may have been due to reduction of clinical effects by intense immunosuppression in presensitized patients. Evaluating CDC, 29% of CDC-PRA(+)/[C4d]FlowPRA(+) recipients had C4d-positive graft dysfunction. For these patients 3-year graft survival was worst, followed by CDC-PRA(+)/[C4d]FlowPRA(-) and CDC-PRA(-) patients (76% vs. 81% vs. 90%, p=0.014). Results highlight a strong impact of complement-fixing HLA presensitization. Discerning complement-activating abilities of HLA alloantibodies, [C4d]FlowPRA may help identify recipients at particularly high risk for graft rejection and loss.

Adult↗
PubMed1986

Diffuse interstitial lung disease in rheumatoid arthritis. Views on immunological and HLA findings.

Immunological parameters including HLA typing were studied in 32 patients with rheumatoid arthritis (RA) associated diffuse interstitial lung disease (DILD) and in 32 age- and sex-matched RA control patients. The male RA patient group with DILD also included patients with other intrathoracic manifestations and had a higher prevalence of HLA-B8 and Dw3 than did healthy controls, thus agreeing with our earlier results that RA patients with this antigen combination are prone to multiple intrathoracic complications. Patients with DILD had higher titres of rheumatoid factor (RF) and lower complement (C4) levels than matched RA controls. The RF titre was in inverse correlation with C3 and C4 levels, suggesting that RF immune complexes may also promote rheumatoid lung disease via activation of the classical pathway of complement.

Aged↗