PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Complement C3a”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1982

Stimulation of the intracellular killing of Staphylococcus aureus by monocytes: regulation by immunoglobulin G and complement components C3/C3b and B/Bb.

The intracellular killing of Staphylococcus aureus by human monocytes requires continuous stimulation by extracellular serum factors interacting with the cells via membrane binding sites. At least 75% of the intracellular killing in the presence of fresh serum was accounted for by the combined stimulatory activities of IgG, C3/C3b, and B/Bb. C3b is a more potent stimulator than C3, and Bb stimulates the killing to the same degree as B. The stimulation of intracellular killing by C3 and C3b occurs by interaction of the stable binding site of this molecule with the C3b receptor in the monocyte membrane. The stimulation of intracellular killing by B and Bb is most probably mediated via a binding site on these proteins interacting with a receptor site in the monocyte membrane. Both complement receptors, i.e., for C3b and B, are pronase sensitive. However, only the C3b receptor can be inhibited by (Fab')2 fragments of anti-C3 receptor antibodies, indicating that the binding sites for C3/C3b and B/bb are different.

Blood Bactericidal Activity↗
PubMed1995

The acylation stimulating protein-adipsin system.

Considerable evidence indicates that obesity, and in particular abdominal obesity, is a risk factor for both heart disease and non-insulin dependent diabetes mellitus. In spite of this, little is known of the regulation of triacylglycerol synthesis in adipose tissue other than by insulin. Acylation stimulating protein (ASP), a human plasma protein, stimulates triacylglycerol synthesis in adipose tissue and is also produced by human adipocytes. ASP may play a physiological role in the regulation of efficiency of adipose tissue fat storage and affect clearance of triglycerides from plasma.

3T3 Cells↗
PubMed1994

The adipsin-ASP pathway and regulation of adipocyte function.

The adipsin-ASP pathway provides a mechanism by which the adipocyte is able to regulate its rate of de novo triglyceride synthesis and reesterification. The adipocyte can synthesize and secrete the three proteins necessary for the formation of the effector molecule, acylation stimulating protein (ASP). ASP increases membrane transport of glucose and the activity of diacylglycerol acyltransferase and by virtue of both of these effects markedly increases the rate of triglyceride synthesis. Awareness of the pathway will allow, we believe, a new understanding of the regulation of triglyceride removal from plasma. Accordingly, the concept of microenvironmental metabolic regulation of triglyceride hydrolysis at the endothelial surface and triglyceride synthesis within the adipocyte will be presented. In addition, the pathogenetic sequence by which dysfunction of this pathway can lead to dyslipoproteinaemia will be reviewed. Emphasis, however, will be placed on the role this pathway may play in the pathogenesis of obesity and the adaptation to negative caloric balance in the obese.

Adipocytes↗
PubMed1995

[The effect of the complement system on the acute reversible rejection of kidney transplants].

Although the involvement of complement in hyperacute renal allograft rejection is well established, its possible implication in acute reversible and chronic graft rejection remains uncertain. In recent clinical studies with a total of 83 patients undergoing renal transplantation, plasma levels of complement activation products were elevated 4-7 days before clinical diagnosis of graft rejection. Immunohistochemical analysis of biopsies revealed local complement activation with glomerular deposition of the terminal C5b-9 complex within 1 h after organ reperfusion. Increasing levels of complement activation products, preceding the clinical manifestation of renal graft rejections may be of diagnostic value in recognizing patients at risk.

Acute Disease↗
PubMed1996

[Adipsin system--acylation-stimulation protein (ASP) and hyperapo-B].

Acylation Stimulating Protein (ASP) is a small basic protein which was isolated from the human plasma and which has been shown to be the most potent stimulant yet discovered of triglyceride synthesis. The initial observation were made in vitro, but there is now in vivo evidence that the adipsina-ASP system has an important regulatory role in triglyceride clearance from plasma. Studies in normals have shown that the higher the fasting and the peak ASP plasma levels are after an oral fat load, the faster the triglyceride clearance from plasma. Moreover, decreased function of the adipsina-ASP system appears to lead to increased delivery of free fatty acids and triglyceride-rich chylomicron remnants to the liver with a consequent increase in the rate of secretion of B100 lipoprotein particles. That is to say, defective function of this system is one of the causes of hyperapoB which in turn is one of the commonest dyslipoproteinemias associated with premature coronary artery disease.

Apolipoproteins B↗
PubMed1999

Immunoglobulin M-enriched human intravenous immunoglobulin prevents complement activation in vitro and in vivo in a rat model of acute inflammation.

An important antiinflammatory mechanism of intravenous immunoglobulin preparations (IVIG) is their ability to block complement activation. The purpose of this study was to compare the complement-inhibitory activity of four IVIG preparations differing in isotype composition. The preparations were: (1) IVIgG (48 g/L IgG, 2 g/L IgA; Intraglobin F); (2) Pentaglobin (38 g/L IgG, 6 g/L IgM, 6 g/L IgA); (3) IVIgM (35 g/L IgM, 12 g/L IgA, 3 g/L IgG); and (4) IVIgA (41 g/L IgA, 9 g/L IgG), all from Biotest Pharma GmbH, Dreieich, Germany. Their complement inhibitory activity was assessed in vitro by measurement of the blocking of C1q-, C4-, and C3 deposition on solid-phase aggregated rabbit IgG by enzyme-linked immunosorbent assay (ELISA). Complement inhibition in this ELISA was best for IVIgM, followed by Pentaglobin and IVIgG; IVIgA did not exhibit an inhibitory effect. Control experiments with excess concentrations of C1q as well as with C1q-depleted serum showed that the inhibitory effects of IVIG were not caused by complement activation and thus, consumption, but that C4 and C3 were scavenged by IgM and to a lesser extent by IgG. These results were confirmed in vivo in the rat anti-Thy 1 nephritis model, in which a single dose of 500 mg/kg of IVIgM prevented C3-, C6-, and C5b-9 deposition in the rat glomeruli, whereas the effect of IVIgG was much less pronounced. Reduction of complement deposition was paralleled by a diminished albuminuria, which was completely absent in the IVIgM-treated rats. IVIgM and to a lesser extent IVIgG also prevented rat C3 deposition on cultured rat glomerular mesangial cells in vitro, but did not influence anti-Thy 1 binding. Neither IVIgM nor Pentaglobin nor IVIgG negatively affected in vitro phagocytosis of Escherichia coli (E coli) by human granulocytes. In conclusion, we have shown that IgM enrichment of IVIG preparations enhances their effect to prevent the inflammatory effects of complement activation.

Animals↗
PubMed2003

A complement component C3a-like peptide stimulates chemotaxis by hemocytes from an invertebrate chordate-the tunicate, Pyura stolonifera.

Recent evidence suggests that the complement system evolved as a critical host defence mechanism among invertebrates, long before the origin among vertebrates of adaptive immune responses mediated by somatically re-arranging antibodies. The current study supports that contention by identifying a complement component C3a-like peptide in the tunicate, Pyura stolonifera. Activation of P. stolonifera serum with common inflammatory elicitors (lipopolysaccharide and zymosan) resulted in the proteolytic generation of an 8.5 kDa peptide, and concomitantly conferred chemoattractant activity on the serum. The 8.5 kDa peptide shares substantial amino acid sequence homology with a previously characterised tunicate complement component C3-like protein (72% amino acid identity in an 18 amino acid overlap). It is also recognised by an anti-C3 antiserum that is known to cross react with tunicate C3 homologues. Hemocyte migration assays performed with the 8.5 kDa peptide that had been partially purified by gel filtration confirmed that the molecule acts as a powerful chemotactic agent. This suggests that the proteolytic activation of tunicate C3-like molecules can initiate inflammatory responses involving cellular recruitment by liberating a pro-inflammatory peptide akin to the vertebrate anaphylatoxin, C3a.

Amino Acid Sequence↗
PubMed1986

[A new case of bronchospasm under extracorporeal circulation].

A case of bronchospasm occurring after the termination of cardiopulmonary bypass is reported. The complement fractions C3a, C4a and C5a were measured before and right after CPB. Complement activation is not specific to CPB but may occur in any thoracotomy. The statistically significant increase in complement C3a without any pulmonary symptomatology has been reported by several authors. Complement activation cannot therefore be considered as the explanation of this bronchospasm.

Bronchial Spasm↗
PubMed1995

Levels of the terminal complement complex, C3a-desArg and C1-inhibitor in adult patients with capillary leak syndrome following bone marrow transplantation.

Capillary leak syndrome (CLS) is a severe complication after bone marrow transplantation (BMT). To investigate whether there is a pathogenetic role of the complement system, we monitored the levels of the terminal complement complex C5b-9 (TCC) and C3a-desArg as indicators of an activation of the complement system and the inhibitor of the classical pathway of the complement cascade, C1 inhibitor (C1-INH), in 48 bone marrow transplant recipients from 1 week before to 5 weeks after transplantation. Capillary leak syndrome developed in 7 out of 48 patients between days 1 and 12 after BMT. Complement activation as indicated by TCC levels was more pronounced in patients with CLS (n = 7) from day -8 to +28 (p < 0.05; day -1) and the elevation of TCC levels lasted longer in CLS patients (peak day 21) than in patients without this complication (peak day 7). Mean C3a-desArg levels were highest in patients with CLS reaching a peak at day 7. During the early posttransplant period a significant elevation of C1-INH levels (p < 0.01 and p < 0.05 respectively) compared with baseline levels (day -8) was found in patients with and without CLS, which was more pronounced in those patients with CLS (p < 0.05). Although we could not observe an absolute C1-INH deficiency as compared to healthy individuals our data support the presence of a relative deficiency of the inhibitor which might explain the reported beneficial effects of C1-INH substitution in BMT related CLS.

Adult↗