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PubMedDate not supplied

[Significance of deposits of immunoglobulins G, A, M and C3 complement component in the basal membrane zone of clinically unchanged skin for the diagnosis and evaluation of systemic lupus erythematosus activity].

Direct immunofluorescent test of clinically unaltered skin, the so-called lupus band test (LBT) was performed in 38 patients with systemic lupus erythematosus. Test was positive in 23 patients or 60.52%, respectively. It was established that the relative number of LBT positive patients was increased, from 37.5% in the group with the lowest disease activity determined by SLEDAI score, over 66.66% in the group with moderate activity till 100% in the patients with extremely active disease. Comparison of SLEDAI score (disease activity) mean values in the group of patients with systemic lupus erythematosus (SLE) with positive LBT compared to the group with negative LBT revealed statistically significant difference (< 0.05) in favour of the first group. No significant disease activity among patients' groups, formed according to the types and number of registered immunoreactants was observed. LBT in patients with SLE should be done in prognostic purposes. Positive LBT indicates the more active disease. Besides, the test can be a valuable diagnostic indicator in patients who do not fulfill the diagnostic criteria of American College of Rheumatology.

Adolescent↗
PubMed1980

Predictive value of serum complement (C3) in renal allograft rejection.

The purpose of this study was to investigate whether or not changes in serum concentrations of complement component C3 are of value in predicting the long term survival of the transplanted kidney. C3 was quantitated by radial immunodiffusion in fresh sera drawn immediately before transplantation and twice weekly thereafter from 10 recipients. Fourteen episodes of acute rejection occurred during the first 3 months postoperatively. These were diagnosed by the demonstration of graft tenderness, fever without evidence of infection and a rise in serum creatinine of 1 mg/dl in the absence of urinary or vascular obstruction. Five rejection episodes in 3 patients were associated with a fall in C3. In one of these patients, C3 returned to normal levels after the episode was reversed, and the kidney is functioning well 2 years after transplantation. In the other 2 patients, C3 remained at low levels regardless of anti-rejection therapy. Transplant nephrectomy was soon required for irreversible rejection. In contrast, only 1 episode unaccompanied by a fall in C3 was irreversible. Evidence is provided concerning the value of serial C3 complement determinations as a predictor of rejection in renal allografts. Using the variability measure Si, the cumulated standard deviation up to week i, Si > 10 not only predicts rejection but does so rather early, providing more than 90 per cent of the ideal lead time. This suggests that loss of a graft may be predicted, but this needs confirmation in additional cases.

Complement C3↗
PubMed1996

Local secretion of complement C3 in the exocrine pancreas: ductal epithelial cells as a possible biosynthetic site.

BACKGROUND & AIMS: The complement system participates in the local immune system in various tissues. In this study, we investigated the local secretion of complement C3 into the pancreatic fluid and attempted to determine a possible biosynthetic site. METHODS: C3 protein in human pancreatic fluid was analyzed by, immunoblotting. The C3 messenger RNA (mRNA) expression in several pancreatic carcinoma cell lines was analyzed by the polymerase chain reaction and/or Northern blotting. The secretion of C3 by these pancreatic carcinoma cells was assessed by metabolic labeling and immunoprecipitation experiments. RESULTS: In five samples of human pancreatic fluid, C3 was detected as a molecule composed of alpha and beta chains. C3 mRNA expression was observed in the ductal cell carcinoma lines (PANC-1 and MIA PaCa-2) but not in the acinar cell line (HPC-YO and AR-42J). C3 production in these cells was enhanced by interleukin 1 beta and tumor necrosis factor alpha at both the protein and the mRNA levels. CONCLUSIONS: (1) Complement C3 is secreted into the exocrine fluids of the pancreas. (2) Ductal epithelial cells are possible biosynthetic sites for C3. (3) The proinflammatory cytokines, interleukin 1 beta and tumor necrosis factor alpha are effective stimulators of local C3 production in the pancreas.

Adult↗
PubMed1976

A family with partial and total deficiency of complement C3.

A young White girl was found to have no detectable complement C3 or C1q. She suffered repeated attacks of pneumococcal meningitis and pneumococcal pneumonia. Her parents, and some of her siblings, had half the normal level of C3; other siblings were normal. She also had decreased IgG levels and increased IgM concentrations. These findings are correlated with a dysmorphic state of the germinal centres of the peripheral lymphoid tissues, seen after death.

Child↗
PubMed1992

[Complement C3 and C4 levels in serum from acute viral hepatitis].

Serial measurements of C3 and C4 complement components were performed in 50 patients with acute, uncomplicated viral hepatitis, in the beginning of the symptoms and in the peaks of serum transaminases. There were 17 patients diagnosed as having Hepatitis A virus (HAV) infection and 33 patients diagnosed as having Hepatitis B virus (HBV) infection. There were 4 women and 46 men with a mean age of 22.1 years. In the sera of 50 healthy control subjects serum C3 and C4 complement components measured, this group was composed of 15 women and 35 men with a mean age of 26 years. The complement component levels were observed to be reduced in both viral infections, where the reduction in C3 serum concentration was found to be statistically significant but reduction in C4 serum concentration was not.

Acute Disease↗
PubMed1998

Biological activities of C3 beta c, a novel neutrophil chemoattractant derived from the beta-chain of rat complement C3.

Biological activities of C3 beta c, which is a C-terminal fragment of the beta-chain of rat complement C3, have been studied by in vivo and in vitro experiments. C3 beta c was purified as a novel neutrophil chemoattractant from the exudate of the chronic phase of rat carrageenin-induced inflammation. The purified C3 beta c induced neutrophil chemotaxis in vivo when C3 beta c was injected into the preformed air-pouch on the back of rats. C3 beta c transiently increased the intracellular free Ca2+ concentration of neutrophils and enhanced the adhesion of neutrophils to fibrinogen in vitro, suggesting that C3 beta c has the ability to express an adhesion molecule of rat neutrophils. In addition, C3 beta c at low concentrations (10(-10)-10(-11) M) stimulated rat macrophages to produce cytokine-induced neutrophil chemoattractant-2, a member of the interleukin-8 family. Furthermore, C3 beta c enhanced vascular permeability in vivo, which is suppressed by cyproheptadine, suggesting that C3 beta c may have the characteristics of an anaphylatoxin. Our results suggest that C3 beta c contributes to oedema formation and neutrophil accumulation at inflammatory sites in rats.

Animals↗
PubMed2005

Complement C3 is a risk factor for the development of diabetes: a population-based cohort study.

Cross-sectional studies have reported strong correlations between plasma levels of complement C3, insulin, and glucose. This prospective study explored whether elevated levels of C3, C4, and other inflammation-sensitive plasma proteins (ISPs; fibrinogen, orosomucoid, alpha1-antitrypsin, haptoglobin, and ceruloplasmin) are associated with the development of diabetes. Plasma proteins were measured in 2,815 nondiabetic healthy men, age 38-50 years, who were reexamined after a mean follow-up of 6.1 years. Diabetes development (n = 123) was studied in relation to baseline levels of plasma proteins. After adjusting for age, screening year, and glucose at baseline, the odds ratio (95% CI) for developing diabetes was 1.00, 2.4 (1.1-5.3), 2.9 (1.4-6.0), and 5.6 (2.8-10.9), respectively, for men with C3 in the 1st, 2nd, 3rd, and 4th quartiles (trend: P < 0.00001). Fibrinogen, haptoglobin, C4, and the number of elevated ISPs were also related to future diabetes in this model. Only C3 was significantly associated with diabetes development after further adjustments for potential confounders, including BMI, insulin, and other inflammatory markers. We concluded that the risk of developing diabetes is related to levels of complement C3.

Blood Glucose↗
PubMed1999

Genetic disruption of the murine complement C3 promoter region generates deficient mice with extrahepatic expression of C3 mRNA.

Genetic deficiencies of the complement protein C3 occur naturally in humans and animal models and have been induced in mice by targeted deletion of the C3 gene. The study of these deficiencies has provided evidence for C3 functions in immune responses. C3 deficient mice were generated by replacing the 5'-flanking region of the C3 gene with the neomycin-resistance (neo) gene. Serum from these mice had no detectable C3 protein or complement activity. Challenge with Streptococcus pneumoniae revealed approximately 2000-fold increase in bacteremia as compared to littermate controls. C3 mRNA was absent in the liver, but it was detected in the lung, kidney, fat tissue, heart and spleen. Metabolic labeling of the lung tissue and peritoneal macrophages showed synthesis of pro-C3, but no post-synthetic intracellular processing of the protein and no secretion of mature C3. cDNA analysis at the cap site indicated that extrahepatic transcription of the targeted gene was initiated in the neo cassette, close to the C3/neo junction and predicted a primary translation product lacking the leader peptide. The data indicate that these mice provide a good animal model for the study of complete C3 deficiencies and a potential probe for tissue-specific C3 gene regulatory elements.

Animals↗
PubMed2001

Regulation by retinoic acid of acylation-stimulating protein and complement C3 in human adipocytes.

Acylation-stimulating protein (ASP), a product of complement C3, stimulates triacylglycerol synthesis in adipocytes. Previous studies have identified transthyretin, associated with chylomicrons, as a stimulator of C3 and ASP production. Since both transthyretin and chylomicrons transport retinyl ester/retinol, our goal was to investigate whether retinoic acid (RA) could be a potential hormonal mediator of the effect. Inhibitors of protein synthesis and protein secretion eliminated the stimulatory effects of chylomicrons on both C3 and ASP production in human differentiated adipocytes, suggesting that de novo protein synthesis and secretion are both required. Incubation with chylomicrons increased C3 mRNA levels (37+/-1.5%). RA alone or with chylomicrons had a stimulatory effect on C3 production (29-fold at 16.6 nM RA) and ASP production. An RA receptor antagonist blocked stimulation of C3 mRNA and C3 secretion by both RA and chylomicrons. Finally, RA and chylomicrons activated a 1.8 kb C3-promoter-luciferase construct transfected into 3T3-F442 and 3T3-L1 cells (by 41+/-0.2% and 69+/-0.3% respectively), possibly via RA receptor half-sites identified by sequence analysis. This is the first evidence documenting stimulation by RA of the C3 gene. Thus we propose RA as a novel cellular trigger in chylomicrons that subsequently results in increased ASP production by adipocytes after a meal.

3T3 Cells↗
PubMed1979

Complement (C3), nutrition, and infection.

Complement (C(3)) was determined and related to various parameters of nutritional status and past infectious disease experience in a group of 53 rural preschool children in North India. Mean complement level was 25% lower than in an age-matched European reference population. Low complement (C(3)) levels were associated mainly with children who were both stunted and wasted, as well as with those who had experienced frequent purulent skin infections in the past.

Child, Preschool↗
PubMed1993

Plasma fibronectin and serum complement C3 levels in chronic active hepatitis following virus "B" versus virus "C" infection.

Plasma fibronectin and serum complement C3 levels were estimated in 30 patients with chronic active hepatitis (CAH) post virus "B" and another 30 patients with CAH post virus "C" as well as 20 normal healthy subjects. Fibronectin level was significantly increased in CAH when compared to normal controls. Moreover, fibronectin level was significantly increased in CAH following virus "C" when compared to CAH following virus "B" hepatitis. Concerning complement C3 there was no significant changes in the different groups studied. We may conclude that CAH following virus "C" may lead to vigorous inflammatory damage than CAH following virus "B" infection.

Adult↗