PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Complement Hemolytic Activity Assay”

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 109 records · Page 6Linked to original sources
PubMedDate not supplied

Inhibiting action human glioblastoma extract on haemolytic complement of human and xenogeneic sera.

The action of some extracts of human glioblastoma of the haemolytic complement of human and xenogeneic sera has been examined. The study suggests that the antigenic products of some human glioblastomas may induce an inhibiting effect on the haemolytic complement of human, as well as xenogeneic (rat and rabbit), sera. The inhibiting action on the xenogeneic sera is indicative of the presence of species-specific antigens or tumor cells, comparable to that of normal tissues.

Animals↗
PubMed1990

Activation of complement by circulating immune complexes isolated from leprosy patients.

Circulating immune complexes isolated from different types of leprosy sera as polyethylene glycol (PEG) precipitates were found to be efficient activators of the alternative pathway of complement. PEG precipitates from BL/LL leprosy patients and those with erythema nodosum leprosum were found to activate both the classical pathway and the alternative pathway of complement efficiently, while PEG precipitates from TT/BT leprosy patients and borderline tuberculoid patients in reaction were found to active the alternative pathway of complement but not the classical pathway. No significant differences were observed between the PEG precipitates from reactional and nonreactional TT/BT and BL/LL patients in their complement activating ability.

Antigen-Antibody Complex↗
PubMed1990

[Sequential changes in serum complement after aneurysmal subarachnoid hemorrhage].

Twenty-one patients were submitted to investigate serum complements (CH50, C3, C4) after aneurysmal subarachnoid hemorrhage during a 2 to 3-week period. As for the control, the same examination was carried out in patients with non-subarachnoid hemorrhage such as hypertensive intracerebral hemorrhage. There was no remarkable changes of serum complements in the control patients. Preoperative grading (Hunt & Hess) was well correlated with C4 level but not C3 level. Ce and C4 level of the patients without symptomatic vasospasm did not change markedly after subarachnoid hemorrhage during the investigation, while they decreased severely in patients with severe vasospasm and major neurological deficit. The patients with mild symptomatic vasospasm without major neurological deficit showed transient decrease of C3 and C4 level in the period of 5 to 10 days after subarachnoid hemorrhage. These data show that sequential determinations of serum complements (C3 and C4) level after subarachnoid hemorrhage is a useful method for the choice of therapy, and for the prognosis of aneurysmal patients after subarachnoid hemorrhage.

Adult↗
PubMedDate not supplied

Alternative complement pathway in hypocomplementemic/normal C1s-C1 inhibitor complex patients with SLE.

To test whether alternative complement pathway activation explains normal C1s-C1 inhibitor complex in hypocomplementemic (low CH50cl) patients with systemic lupus erythematosus, we examined alternative pathway hemolytic complement (CH50alt) factor B, and Ba fragment in hypocomplementemic sera with normal and with elevated C1s-C1 inhibitor complex. Sera with and without high C1s-C1 inhibitor complex were similar in CH50cl, C3, and C4. There was little evidence for important alternative complement pathway activation in either group, but patients with classical pathway activation (elevated C1s-C1 inhibitor complex) had slightly lower CH50alt and slightly higher factor B and Ba compared to patients with normal C1s-C1 inhibitor complex. Pregnant patients did not differ from non-pregnant patients. Alternative complement pathway activation does not account for hypocomplementemia in this group of patients.

Complement Activation↗
PubMed1990

[Plasma levels of complement fragments during hemodialysis in patients with chronic renal failure].

The kinetics of hemodialysis-induced leukopenia and generation of complement fragments including C3a, C5a, C4d, iC3b and Bb were investigated in 14 patients during hemodialysis using cellulose acetate (CA), cuprophan (Cu) and ethylenevinyl alcohol (EVA) membranes. A marked leukopenia in the first 15 minutes was observed in CA and Cu. Plasma C3a levels were higher in CA than in Cu and EVA. Plasma C5a levels were higher in CA and Cu than in EVA. There was a negative correlation between the white blood cell counts and plasma C5a levels at 15 minutes (gamma = -0.85, p less than 0.001). Plasma C4d levels showed no increase in all membranes. Plasma iC3b levels were higher significantly in Cu than in CA and EVA. Plasma Bb levels in the first 15 minutes increased significantly in all membranes, and furthermore continued to increase till the end of hemodialysis in CA and Cu. This study revealed that all the membranes tested activated the complement via the alternative pathway to produce Bb, iC3b, C3a and C5a. C5a was thought to take an important role in transient leukopenia. Furthermore, Bb was accumulated during hemodialysis in CA and Cu, and its biological effects on patients undergoing hemodialysis should be studied.

Adult↗
PubMed1989

[Major complement inhibiting factors from the venom of the Central Asian cobra Naja naja oxiana].

The properties of two anticomplementic factors isolated by CM-Sepharose chromatography from the basic non-adsorbed on DEAE-Sepharose fraction of the Central Asian cobra Naja naja oxiana venom, were studied. Of these three factors (CFB-I, CFB-II and CFB-III) the latter had been characterized earlier. CFB-I was shown to be a protein with an N-terminal Asp and a molecular mass of about 39 kDa (data from gel chromatography); its content in the venom is 3.6 mg/g of dry venom. The protein inhibits mainly the classical pathway of the complement activation, being bound to component C4 (Ki = 9 nM). CFB-I seems to be analogous to the CI inhibitor from the venom of the Naja haje cobra. An analysis of the N-terminal sequence of CFB-II showed it to be identical to the earlier characterized cytotoxin I. CFB-I inhibits the formation of C3 convertase with Ki = 2.2-2.8 microM by way of binding to C4b and thus interfering with the component C2 sorption.

Animals↗
PubMed1989

[Clinical significance of the estimations of complement and immune complexes].

Immune complexes (IC) interacting with complement (C) induce tissue injuries and the estimations of their sequential serum levels is clinically significant. In C, among the various parameters, total hemolytic activity (CH 50) is clinically the most useful especially in the diagnosis and treatment of SLE. Elevation of serum CH 50 levels is nonspecifically observed in patients with inflammations and malignancies, although its mechanism remain obscure. Decreased CH 50 levels were observed in various diseases including liver diseases, collagen diseases, kidney diseases, congenital C component deficiencies and so on. Among them, chronic liver disease is the most frequently encountered disease. Liver function should be checked first in cases with low CH 50. In IC, patho-etiological significance has been established and various methods for the estimation have been employed. However, their sensitivities and specificities are various and positivities obtained by these methods vary with the diseases. Clinical significance of IC estimation has been recognized to be limited to a few diseases including SLE, in which some clinical signs parallel the IC level. However, recent developments in the methods employing murine monoclonal antibodies to C1q and C3d and IgG rheumatoid factor are expected to help re-evaluation the significance of serum IC estimation in various diseases. Heat-pretreatment of sera at 56 degrees C or below produced the reactivity of IgG with rheumatoid factors. Therefore, serum samples should be estimated without heat-inactivation.

Antibodies, Monoclonal↗
PubMed1989

Distribution of complement in the sclera.

In the present study, we compared hemolytic activities of C1, C4, C2, C3, C5, C6 and C7 in the anterior and posterior sclera. Additionally, we used radial immunodiffusion to measure levels of Factor B, IgG, IgA and albumin in the anterior and posterior sclera. Except for C1, complement levels were significantly higher in the posterior than anterior sclera. Additionally, levels of immunoglobulins as well as albumin were significantly higher in the posterior than anterior sclera. These results suggest that the posterior sclera has a better adjacent vascular supply than the anterior sclera. On the other hand, the results of this study show that the anterior sclera has more C1, the recognition unit of the classical pathway, than the posterior sclera. Because there is nearly twice as much C1 in the anterior sclera, it may be easier for antigen-antibody complexes, whether formed in the sclera itself or derived from the neighboring vessels, to set off the complement cascade in the anterior sclera. This finding may help explain why scleritis associated with immune complex disease is more common in the anterior than posterior sclera.

Adult↗
PubMed1989

Complement activity and selected hematologic variables in newborn foals fed bovine colostrum.

Serum complement activity and selected hematologic variables were evaluated in 5 newborn foals fed bovine colostrum (principal group) and 6 foals allowed to nurse their dam (control group). Also, bovine colostrum was evaluated for anti-equine antibodies. Precolostral serum hemolytic and conglutinating complement activities were low and increased similarly in foals of both groups to reach adult values between 1 and 3 weeks after birth. Bovine colostrum strongly agglutinated, but did not hemolyse principal foals' RBC and blood containing all known equine blood group alloantigens. Hemolysis was not detected after administration of bovine colostrum. Physiologic anemia developed in foals of principal and control groups during the first week of life. Erythrocyte osmotic fragility in foals of the principal group prior to and after the ingestion of colostrum remained unchanged. However, at 36 hours after birth, there was a significant decrease in erythrocyte osmotic fragility in foals fed homologous colostrum.

Animals↗
PubMed1987

The effects of capsaicin denervation on leucocyte and complement components of the inflammatory response.

Primary afferent unmyelinated nerves containing substance P modulate the inflammatory response to injury through a process known as neurogenic inflammation. Rats treated as neonates with capsaicin, to destroy these nerves permanently, have a reduced capacity to mount an inflammatory response as measured by swelling or plasma extravasation. In this study we examined some aspects of the immunological response to injury in capsaicin-treated rats. One question addressed was whether changes in the inflammatory response are due to abnormal innervation or to a direct toxic effect of capsaicin. It was observed that the histological appearance of thymus, splenic white pulp and popliteal lymph nodes was unaltered in capsaicin-treated rats. However, there was an increase in leucocyte number in splenic red pulp. There was also an increase in the white cell numbers in the peripheral circulation (7 +/- 1 X 10(6)/mL for normal rats and 14 +/- 2 X 10(6)/mL in capsaicin-treated rats, p less than 0.001, Student's t-test). This affected all white cell subgroups. Complement levels in capsaicin-treated rats were not different from normals and both groups showed a similar depletion 6 days following antigenic stimulation with sheep red cells. These data support the view that the reduced cellular response to injury in the capsaicin-treated rat is secondary to the effect of the chemical on afferent nerves and not to a primary toxic effect on cells of the inflammatory response.

Animals↗
PubMed1994

Complement system and host defense against staphylococcal endophthalmitis.

PURPOSE: The authors studied the role of the complement system in host defense against Staphylococcus epidermidis and S. aureus endophthalmitis. METHODS: Guinea pigs in the S. epidermidis model received an intravitreal injection of 7000 viable organisms, and guinea pigs in the S. aureus model received 50 viable organisms. The experimental animals in each model were decomplemented with intraperitoneal (IP) injections of cobra venom factor, whereas the control animals received IP injections of normal saline. Mean log bacterial counts in the vitreous and mean serum complement titers were compared in the experimental and control animals in each model on days 1, 2, 3, and 7. RESULTS: In the S. epidermidis model, mean log bacterial counts in the vitreous were significantly higher in the experimental group than the control group on days 1 and 2 (P < 0.01) and on day 3 (P < 0.05). Mean serum complement titers were significantly lower in the experimental group at all days (P < 0.01). In the S. aureus model, mean log bacterial counts in the vitreous were significantly higher in the experimental group than the control group on day 2 (P < 0.05) and day 3 (P < 0.01). Mean serum complement titers were significantly lower in the experimental group on days 1, 2, and 3 (P < 0.01), but not on day 7. CONCLUSION: These results suggest that decomplemented guinea pigs show impaired host defense to S. epidermidis and S. aureus endophthalmitis and that this defense is restored as complement levels approach normal.

Animals↗
PubMed1994

Paradoxical reconstitution of complement activity following plasma transfusion of an individual with deficiency of the seventh component of complement.

A subject deficient in the seventh component of complement (C7) was plasmapheresed with 660 ml C7-sufficient plasma. The expected reconstitution of C7 activity, followed by exponential decay, was not observed. During day 1, serum haemolytic C7 and total haemolytic complement were undetectable and C7 levels were very low by C7 ELISA. However, low levels of circulating fluid phase terminal complement complex (TCC) were detected. On day 2 about microgram C7/ml serum was detected and this rose to 6 micrograms/ml by day 17. Functional complement activity was also present. At day 28 the serum C7 and total haemolytic complement had dropped to pretransfusion levels. A low level of C5b6 was present in pretransfusion serum and this increased markedly immediately following transfusion when the patient's serum also acquired C7 consuming activity. Throughout the study low levels of anti-C7 antibodies were present but there was no evidence that antibody was directly responsible for the C7 consumption. Nevertheless antibody-antigen interactions could have generated circulating C5b6. C5b6 has been shown previously to have the capacity to inhibit C7 activity in vitro. Investigations of the C7 circulating on days 2-17 demonstrated normal molecular weight, functionally active C7. The donor sera and the recirculating C7 allotyped C7-1 by isoelectric focusing; however, the recirculating C7 showed additional weak bands with C7 functional activity, suggesting a possible genetic or acquired abnormality. Although the disappearance of C7 immediately post-transfusion may be explained by the presence of C5b6, there is no satisfactory explanation for the rising C7 levels on days 2-17 and we cannot exclude temporary C7 secretion by the patient.

Adult↗
PubMedDate not supplied

Terminal complement complex in blood of patients with neurological diseases.

The local involvement of complement (C) in the pathophysiology of tissue lesions in several neurological diseases is known, but it has never been studied whether or not in neurological disorders the C activity in the circulation is altered as well. This was the aim of the present investigations. We measured in blood plasma, with an automatic device for analysis and quantitation of the haemolytic activity of the terminal complement complex, the variables T1, T2 and T3 which define the latter quantitatively. We did this, on the one hand, in 100 patients who had 46 neurological disorders systematized in 16 nosological groups, and, on the other hand, in a control group of 40 healthy blood-donors. The mean values of all variables found in the patients have not been statistically different from those found in the controls. This demonstrates that in neurological disorders possible activations of C remain restricted to the local tissue lesions and do not occur in blood, probably due to the opposition against C activation of the known inhibitor system.

Complement Hemolytic Activity Assay↗
PubMed1993

Use of C6-deficient rats to evaluate the mechanism of hyperacute rejection of discordant cardiac xenografts.

C plays a critical role in the hyperacute rejection (HAR) of discordant xenografts (Xg), but the relative contribution of early vs late C components is unknown. In this study, genetic differences in C6 activity were correlated with HAR of guinea pig cardiac Xg by the rat. Seven rat strains were tested for C activity. Six strains (PVG.R1 (R1), PVG.1A (1A), DA, W/F, F344, LEW) had readily detectable C activity in the total and alternative pathways. Some PVG rats also had adequate C activity [PVG (C+)] but others [PVG (C-)] had a profound C6 deficiency. All rats with adequate C activity (n = 35) rejected cardiac Xg between 15 and 80 min. PVG (C+) (n = 6) rats also rejected cardiac Xg hyperacutely (26 +/- 12 min), whereas PVG (C-) (n = 16) rats, which had high preformed IgM natural antibody titers, rejected cardiac Xg in 1 to 2 days (2678 +/- 542 min). Transfer of serum from R1 rats to PVG (C-) recipients with vigorously beating Xg caused HAR of cardiac Xg within 116 +/- 75 min. Transfer of fresh PVG (C-) serum or heat-inactivated R1 serum did not induce HAR. HAR was characterized by intravascular platelet aggregation and interstitial hemorrhage, whereas Xg transplanted to PVG (C-) recipients had patent vessels at 30 min but were heavily infiltrated by granulocytes and monocytes at 2 days. These findings indicate that a deficiency in C6 prevents HAR but allows an accelerated acute rejection that may be mediated by the generation of vasoactive and chemotactic C3a and C5a.

Animals↗
PubMedDate not supplied

Changes of serum complement and of circulating immune complexes in patients with multiple sclerosis.

The changes of total hemolytic complement (CH50), of C3 and C1q components and of the circulating immune complexes (CIC) were studied in a group of 112 patients with multiple sclerosis (MS) and in 50 controls. The attack was taken as a basis of observation. It was observed that in MS attacks CH50, C3 and C1q were decreased owing to the activation of the complement in the classical way. The CH50 values were found well enough correlated with C3 and C1q (r = 0.535) and respectively r = 0.497) and clearly correlated with the CIC values (r = 0.907). A sharp decrease of CH50 increases the probability of the appearance of an attack with slow remission and the probability of an attack with slow remission is the greater, the greater the increase of CIC values. Low CH50, C3 and C1q values correlated with high CIC values may be considered markers of severity in MS.

Adolescent↗