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Results for “Complement Hemolytic Activity Assay”

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PubMed2005

Serum haemolytic complement levels in German Dahlem Red chickens are affected by three major genes (naked neck, dwarf, frizzled) of tropical interest.

German Dahlem Red chickens with three different major genes of tropical interest: Nana- (naked neck), Ff- (frizzled) and dw- (dwarf), respectively, were tested for serum haemolytic complement, which is essential in innate host defence against infectious agents. Eight different combinations of genes for body size and feather coverage were evaluated. Significant differences both for both the calcium-dependent (classical, CPW) and the calcium-independent (alternative, APW) complement titres were found between the phenotypes. Phenotype nanaffDw- showed the highest complement status. The frizzled (Ff-) gene had a negative influence on APW titres, whereas the dwarf (dw-) gene had a negative influence on CPW titres. The naked neck (Nana-) gene had various influences on the haemolytic complement status. All tested hens had MHC (B) 21 haplotypes, whereas the gene for dwarfism appeared to be linked with the B19 haplotype. It was concluded that introducing major genes (Nana-, dw-, Ff-) to conquer environmental stress in hot climates can have a negative impact on certain aspects of the innate immunity of poultry.

Animals↗
PubMed2005

Haemolytic complement activity and humoral immune responses to sheep red blood cells in indigenous chickens and in eight German Dahlem Red chicken lines with different combinations of major genes (dwarf, naked neck and frizzled) of tropical interest.

A total of 376 chickens from different ecotypes were immunized with the non-pathogenic multi-determinant antigen sheep red blood cells (SRBC). The ecotypes included indigenous chickens from various locations in Tanzania (n=102), India (n=86) and Bolivia (n=89). In addition, eight German Dahlem Red (GDR) chicken lines with different major genes (dwarf, naked neck and frizzled) of tropical interest were also immunized with SRBC. Immune competence of the breeds was assessed by measuring complement haemolytic activity, both from the classical calcium-dependent complement pathway (CPW) and alternative calcium-independent complement pathway (APW), alongside IgTotal, IgG and IgM antibody responses to SRBC at 7 days post immunization. Large variations in complement activity and antibody responses to SRBC were observed within and between the indigenous breeds. Many indigenous chickens, especially from Bolivia, showed decreased complement activity (APW) following immunization with SRBC. Breeds from India showed the highest CPW activity and humoral (especially IgM) responses to SRBC, suggesting high immune competence. In contrast, Bolivian chickens were characterized by low CPW activity, low APW activity and low antibody levels to SRBC suggesting an overall low immune competence. In the GDR chickens, characterized by high CPW activity and high IgG antibody responses to SRBC, the major genes for naked neck, frizzling and dwarfism had no significant effect on the antibody responses and complement activity to SRBC.

Animals↗
PubMed1999

Rapid selection of complement-inhibiting protein variants in group A Streptococcus epidemic waves.

Serotype M1 group A Streptococcus strains cause epidemic waves of human infections long thought to be mono- or pauciclonal. The gene encoding an extracellular group A Streptococcus protein (streptococcal inhibitor of complement) that inhibits human complement was sequenced in 1,132 M1 strains recovered from population-based surveillance of infections in Canada, Finland and the United States. Epidemic waves are composed of strains expressing a remarkably heterogeneous array of variants of streptococcal inhibitor of complement that arise very rapidly by natural selection on mucosal surfaces. Thus, our results enhance the understanding of pathogen population dynamics in epidemic waves and infectious disease reemergence.

Animals↗
PubMed1994

Clusterin depletion enhances immune glomerular injury in the isolated perfused kidney.

Clusterin is a normal plasma protein, shown to be an inhibitor of reactive complement hemolysis and a component of the fluid phase SC5b-9 terminal complement complexes. It is a component of glomerular immune deposits in human and experimental glomerulonephritis. Using the complement-dependent isolated perfused rat kidney model of autologous phase passive Heymann nephritis, we have studied the effect of clusterin depletion of perfused plasma on the development of glomerular injury. Kidneys with planted glomerular sheep anti-rat Fx1A antibody were perfused with human plasma either depleted of clusterin to < or = 30%, or control plasma depleted of plasma fibronectin. Glomerular injury was then initiated by the addition of guinea pig anti-sheep immunoglobulins to the perfusate. Kidneys perfused with clusterin depleted plasma developed significantly greater proteinuria at all time points when compared to control kidneys. Glomerular antibody binding and C3 deposition were similar in the two groups, but terminal complement components were deposited in larger amounts in the clusterin depleted group. These data support a possible role for clusterin in vivo in the protection of complement-induced glomerular injury.

Animals↗
PubMed1997

Renal microvascular injury induced by antibody to glomerular endothelial cells is mediated by C5b-9.

We have recently developed a model of thrombotic microangiopathy with injury to the glomerular endothelial cell (GEN) induced by heterologous antibody to rat GEN. In addition to GEN injury rats developed glomerular platelet aggregation and fibrin deposition, acute renal failure, and acute tubular necrosis with interstitial inflammation. To study the role of complement in mediating this lesion, we induced the disease in normal complement PVG rats and measured the effects of generalized complement depletion with cobra venom factor (CVF) and of selective C6 deficiency using genetically C6 deficient PVG animals. Complement sufficient rats developed severe endothelial injury accompanied by platelet aggregation, fibrin deposition, decrease in endothelial cells assessed by antibody staining in the glomerulus, and macrophage infiltration. These changes were associated with marked reduction in renal function. These features were either absent or markedly diminished in complement depleted or C6 deficient rats. This demonstrates that C5b-9, the terminal product of activation of the complement cascade, plays an important role in the pathogenesis of this immune renal microvascular endothelial injury model. Thus, the complement system may play a pathogenic role in renal microvascular diseases such as thrombotic microangiopathy.

Acute Kidney Injury↗
PubMed1998

Involvement of the complement system in antibody-mediated post-exposure protection against human immunodeficiency virus type 1.

We previously reported that passive transfer of a murine V3-specific monoclonal antibody (BAT123) to hu-PBL-SCID mice challenged with HIV-1LAI confers postexposure protection from infection. The role of the Fc fragment of this antibody as well as the involvement of the complement system in protection were evaluated in vivo. When we compared the postexposure protection offered by BAT123 and CGP 47439, a chimeric form of BAT123 in which the murine Fc domain has been replaced by a human IgG1 Fc domain, CGP 47439 failed to provide postexposure protection against HIV-1LAI despite having similar pharmacokinetics and in vitro neutralizing activity. Furthermore, when hu-PBL-SCID mice were treated with cobra venom factor, which inactivates serum complement activity, the postexposure protective ability of BAT123 was abrogated. These findings suggest that the complement system is involved in the passive protection against HIV-1 infection conferred by the murine monoclonal antibody BAT123 in hu-PBL-SCID mice.

Animals↗
PubMed1990

Patterns of immune response among survivors of group B streptococcal meningitis.

Serum samples from 10 infants surviving type III, group B streptococcal (GBS) meningitis were collected acutely and longitudinally for 6 months to determine patterns of antibody response to the capsular polysaccharide and their in vitro functional correlates. Five infants who failed to develop specific antibody at a mean of 3.8 weeks after diagnosis had an increase of greater than or equal to 1.0 microgram/ml after another 4-8 weeks. This IgM-predominant type-specific antibody declined to baseline 2-4 months later. Opsonophagocytosis of type III GBS increased from 0 to 88% in parallel with peak antibody response. Three infants developed increased antibody and opsonophagocytosis at 15-31 weeks after diagnosis, while two had no detectable response. Despite increasing complement levels, opsonophagocytosis of type III GBS was poor with low specific antibody levels These results suggest that survivors of GBS meningitis transiently develop specific antibody and associated efficient opsonophagocytosis, but functional competence does not persist despite maturation to adult levels of complement proteins.

Aging↗
PubMed1998

Complement-mediated cytolysis and azidothymidine are synergistic in HIV-1 suppression.

Some normal human sera contain a natural IgM antibody against gangliotetraose and GM2 which is capable of initiating complement-mediated cytolysis of HIV-1-infected cells. A potent cytolytic serum (lytic serum) harboring this antibody also caused lysis of HIV-1 virions. When lytic serum was added to a mixed culture of HIV-infected cells and naive cells at a ratio of 1:100, expansion of HIV-1 infection was postponed by 1 week. Furthermore, the co-presence of both the lytic serum and azidothymidine continued to significantly suppress infection, even after 4 weeks of cultivation.

Anti-HIV Agents↗
PubMed2004

Hypocomplementaemia as an immunological marker of morbidity and mortality in patients with primary Sjogren's syndrome.

OBJECTIVE: To analyse the prevalence and clinical significance of hypocomplementaemia in a large series of patients with primary Sjogren's syndrome (SS), focusing on the association of low complement levels with clinical manifestations, immunological features, lymphoproliferative disorders and mortality. METHODS: Complement determinations (C3 and C4 levels, CH50 activity) were made in 336 consecutive patients with primary SS (313 women and 23 men, mean age 58.5 yr). We also analysed complement levels in 46 patients with SS associated with hepatitis C virus (HCV) infection and 184 with HCV-related cryoglobulinaemia as control groups. RESULTS: Hypocomplementaemia was detected in 81 (24%) of patients with primary SS, low CH50 being detected in 51 (15%), low C3 values in 42 (12%) and low C4 values in 39 (12%). In the multivariate analysis, patients with low C4 levels showed a higher prevalence of peripheral neuropathy, cutaneous vasculitis, RF, cryoglobulins and lymphoma compared with those with normal C4 levels. The analysis of the 218 SS patients followed prospectively since 1994 showed a lower probability of survival in patients with hypocomplementaemia (with low C3, C4 or CH50 levels) at protocol entry. SS-HCV patients presented a higher frequency of hypocomplementaemia than patients with primary SS (76 vs 24%, P<0.001); nine (20%) of these patients had persistent, unquantifiable complement levels. CONCLUSION: Hypocomplementaemia is closely associated with systemic expression and adverse outcomes (lymphoma development and death) in patients with primary SS. Our results support the inclusion of complement determination at diagnosis as a predictor of the outcome of patients with primary SS and its routine determination in the clinical follow-up.

Aged↗
PubMed1993

A biologic basis for altered host defenses in surgically infected abscesses.

OBJECTIVE: This study determines whether there are any differences in several immunologic parameters in circulating peripheral blood leukocytes, serum, and plasma compared with pus leukocytes, and supernatant of various types of abscess. SUMMARY BACKGROUND DATA: Although there have been reports of high lysozyme levels and low complement levels within pus, there has been no systemic comparison of concentrations of these substances and others within pus compared with those within peripheral blood. METHODS: Peripheral blood and abscess pus were collected from 31 patients with abscesses and percent and mean channel of monocytes expressing complement receptor and major histocompatibility antigen HLA-DR, the percent and mean channel of polymorphonuclear leukocytes (PMN) expressing complement receptor, lysozyme level, and levels of total hemolytic complement, iC3b, C5b-9, and immunoglobulins were measured within both pus and peripheral blood. RESULTS: Percent of monocytes expressing HLA-DR and percent of monocytes and PMN expressing complement receptor, total hemolytic complement, and IgM were reduced within pus compared with peripheral blood, whereas the mean channel of monocytes expressing HLA-DR and the mean channel of PMNs expressing CR3, C5b-9, and lysozyme were increased in pus. CONCLUSIONS: There are marked differences in immunologic parameters measured within pus of abscesses versus that seen in peripheral blood.

Abdomen↗
PubMedDate not supplied

Activation of plasma components by leukocyte removal filters.

The technique of leukocyte filtration has been introduced into cardiac surgery to reduce leukocyte mediated reperfusion injury. When autologous whole blood (WB) is used as filtrate, it is more likely to be activated by the filter material than are banked red blood cell concentrates (RCC), because of its richness in plasma components. This study was designed to compare the activation of plasma components during leukocyte filtration from WB (n = 10) taken from the heart-lung machine, with RCC (n = 10) obtained from the blood bank. Leukocyte filters made from either cellulose acetate or polyester were used. Blood samples were taken simultaneously from the inlet and outlet of the filter after filtration of either 700 ml of WB or 350 ml of RCC. Results indicated that the complement cascade was activated, as reflected by the increase of C3a and C5a during filtration of WB by filters made from cellulose acetate. In contrast, there was no significant increase of C3a and C5a during filtration of RCC. The clotting system, indicated by fibrinopeptide A, and the fibrinolytic system, indicated by fibrinogen degradation products, were not activated during leukocyte filtration. These data suggest that it is the WB taken from the heart-lung machine rather than the RCC from the blood bank that is being activated during leukocyte filtration. Thus, careful selection of filter material is important for leukocyte filtration of autologous whole blood during cardiac surgery.

Cellulose↗
PubMed1996

Role of Fc fragments in inhibition of xenogenic hyperacute rejection by intravenous immunoglobulin.

It has been shown that a high dose administration of human intravenous immunoglobulin G (IVIG) prolonged the survival time of xenografted guinea pig heart in the rat. In this study, we compared the effectiveness of intact IVIG (I-IVIG), Fc fragments of IVIG (Fc-IVIG), and F(ab') fragments of IVIG (Fab-IVIG) in preventing xenogenic hyperacute rejection in the guinea pig-to-rat heart transplantation model. Relatively high dose administration of IVIG (0.6 g/kg body weight) induced xenograft survival times of 32.0 +/- 13.0 min and 33.2 +/- 16.8 min with I-IVIG and Fab-IVIG, respectively, which were significantly longer than times for animals treated with Fc-IVIG or for untreated control animals (survival times of 12.6 +/- 7.4 min and 10.4 +/- 7.6 min, respectively). The in vitro inhibitory effect of guinea pig red blood cell hemolysis by fresh rat serum correlated with the results of in vivo study. On the other hand, the in vitro inhibitory effect of IVIG on pig red blood cell hemolysis by fresh human serum showed that Fc-IVIG, which had little effect in the guinea pit-to-rat combination, had a higher inhibitory effect than Fab-IVIG, or I-IVIG. Fc-IVIG and I-IVIG achieved a complete inhibition of in vitro hemolysis in the pig-to-human combination. It is suspected that an interference with the complement classical pathway by the Fc portion of IVIG could be an attractive tool for inhibition of hyperacute rejection in the pig-to-human combination.

Acute Disease↗
PubMed2003

Accommodation after lung xenografting from hamster to rat.

BACKGROUND: Long-term xenograft survival can be achieved in hamster hearts transplanted into rats treated with cobra venom factor (CVF) and cyclosporine A (CsA). This phenomenon of "accommodation" is associated with expression of protective genes such as bcl-2, bcl-X(L), and heme-oxygenase-1. We examined whether accommodation could be induced in hamster-to-rat lung xenografts and whether the pattern of protective genes is similar to cardiac xenografts. METHODS: We used hamster-to-rat cardiac and lung xenotransplantation models. Cardiac xenotransplants were treated with CVF+CsA and compared with untreated controls. Lung xenotransplants were treated with either CVF+CsA or FK506 and cyclophosphamide (Cp) and compared with untreated controls. All recipients were killed by 21 days after transplantation. We examined graft survival and protein expression of protective genes, and we performed histologic and immunohistologic analyses. RESULTS: Rejection occurred rapidly in untreated rats. CVF+CsA or FK506+Cp treatment significantly influenced graft survival. Eight of 12 CVF+CsA-treated heart transplants survived 21 days. Seven of 16 CVF+CsA-treated lung grafts and five of 12 FK506+Cp-treated lung xenografts survived 21 days. We observed significant protein expression of bcl-2, bcl-X(L), and heme-oxygenase-1 in cardiac xenografts treated with CVF+CsA at 2, 14, and 21 days after transplantation, compared with normal hamster hearts. We also observed significant expression of these proteins in lung xenografts treated with either CVF+CsA or FK506+Cp at 21 days after transplantation, compared with normal lungs. CONCLUSIONS: Accommodation may be a general phenomenon for all organs, mediated through protective genes. Induction of accommodation does not require disruption of the complement system.

Adaptation, Physiological↗
PubMed1990

Complement, complement activation and anaphylatoxins in human ovarian follicular fluid.

Functionally active complement was sought and detected in human follicular fluids obtained during the pre-ovulatory period. All the functional complement activities tested, including total haemolytic complement, classical pathway activity and alternative pathway activity were present in nine fluids from four different donors with values within the normal serum range. The immunochemical analysis demonstrated the presence of complement factors from C1 to C9, of B and of C1 INH, H, I. Complement anaphylatoxins were found employing RIA techniques in amounts significantly higher than in human plasma, thus demonstrating that follicular fluid complement, at least during the pre-ovulatory period, is partially activated. A possible role for urokinase-like substances in such an activation was indicated by further in vitro experiments. The presence of active complement in follicular fluid can be relevant for the function of the enzymatic multi-factorial mechanism of ovulation.

Anaphylatoxins↗
PubMed1993

An acute model for IgA-mediated glomerular inflammation in rats induced by monoclonal polymeric rat IgA antibodies.

An acute model for IgA-mediated glomerular inflammation in rats was induced by the in situ deposition of IgA directly into the glomerular mesangium. F(ab')2 anti-Thy1 MoAb was used to anchor an antigen, DNP (2,4-dinitrophenol), in the glomeruli of rats. Subsequent infusion of rat polymeric (p-) or monomeric (m-) IgA MoAb with specificity for DNP resulted in mesangial deposition of IgA in both groups of rats. However, acute proteinuria was observed only in p-IgA-treated rats and not in PBS- or m-IgA-treated rats. Immunofluorescence analysis revealed deposition of C3 in an identical pattern to that of IgA in the glomeruli of p-IgA-treated rats. No mesangial deposits of C4 or C1q were seen in these animals. Rats receiving m-IgA or PBS displayed no detectable C3, C4 or C1q deposition. The amount of proteinuria in p-IgA-treated rats was related to the amount of deposited C3. The presence of intraglomerular monocytes was only observed 2 days after p-IgA injection. By light microscopy, aneurysm formation, mesangial hypercellularity and matrix expansion were seen only in p-IgA-treated rats. However, by 37 days post-injection complete resolution of the lesions was observed. No histological renal changes were observed in PBS- or m-IgA-treated rats. In conclusion, an acute form of IgA-mediated nephritis in rats was induced by p-IgA but not by m-IgA. This reproducible model provides a basis for further study into the mechanisms of IgA-mediated glomerular inflammation.

2,4-Dinitrophenol↗
PubMed1993

Multifunctional effects of anticomplementary agent K-76 on carrageenan-induced colitis in the rabbit.

In this study the effect of K-76, a sesquiterpene compound with anticomplementary activity isolated from a fungus culture, on carrageenan-induced colitis was studied from biochemical, histological and immunohistopathological aspects. K-76 suppressed epithelial cell loss, crypt abscess formation, inflammatory cell infiltration, mucosal atrophy, and ulceration. Immunohistochemical examination of the colonic mucosa showed that the number of IgG- and IgM-positive plasma cells and the staining intensity for IgG and C3 were increased in carrageenan-induced colitis, but these changes were inhibited by K-76. Besides, serum mucoprotein concentrations and CH50 levels were lower in the animals treated with carrageenan alone. K-76 exerted multifunctional activity, although its mechanisms of action remain obscure.

Animals↗