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PubMed1989

The complement system in the acute phase of myocardial infarction.

Although some studies suggest that complement activation is involved in the development of acute myocardial infarction, there has been little convincing evidence of a change in the complement system in patients suffering from myocardial infarction. In this study circulating levels of C3a, C3, C4 and the total hemolytic complement titer (CH50) were serially measured in 12 patients with acute myocardial infarction up to 10 days after an attack. The plasma C3a level was greatly elevated throughout the post-attack observation period. The C3, C4 and CH50 levels were significantly increased above those controls on days 8, 9 and 10 after infarction. These findings indicate that there is complement activation in patients with acute myocardial infarction, and suggest a pathogenetic role for complement activation in the development of myocardial damage after infarction.

Acute-Phase Reaction↗
PubMed1992

[A study of the humoral immunity of mice injected with beryllium chloride].

We studied changes of humoral immunity, such as complement pathway activity, C3 contents and contents of immunoglobulin, in mice injected subcutaneously with BeCl2 or CuCl2 once a week for 12 weeks. Mean body weights of JCL: ICR female mice were approximately 30g in control mice (control group; n = 7), in mice injected with Be (Be group; n = 8) and in mice injected with Cu (Cu group; n = 8). Values of classical complement pathway activity (CH50) were 18.8 +/- 1.4 U per ml, 15.3 +/- 1.8 U per ml and 16.7 +/- 1.3 U per ml in the control group, Be group and Cu group, respectively. The CH50 values of Be and Cu groups were significantly lower than that of the control group (P < 0.01). In contrast, values of alternative complement pathway activity (ACH50) and contents of C3 were almost constant in the three groups. The immunoglobulin content in the Be group tended to increase. The activity of alanine aminotransferase in the Be group was markedly higher than that in the control group (P < 0.05), and the aspartate aminotransferase activity was also high. The CH50 value of mice injected with a small amount of Be once a week over a 12-week period decreased markedly, although either the ACH50 value or C3 content was the same as in the control group. The immunoglobulin content somewhat increased in the Be group. These results suggest the possibility that immune complex is induced by Be.

Animals↗
PubMed1992

[Rapid micromethod for CH50 determination using an algorithm].

The titration of haemolytic complement in biological liquid cause inconvenient in calculating concentration, it was long and fastidious. We report a fast technic based on measure of hemolysis in microplate++ method, which exploitation of results, it does with an appropriate algorithm.

Algorithms↗
PubMedDate not supplied

[The action of karbogal on the complement system under model conditions and in an animal experiment].

The influence of dimethylperfluorocyclohexane (carbogal) on the hemolytic activity of human blood serum complement was studied in vitro. It has been show that different effects of carbogol on the complement depend on the serum lipid composition. Endotracheal administration of carbogal to rats results in a significant reduction of complement activity in the animal's blood. Significant changes in the hemolytic activity of the complement recorded 21 days after the endotracheal administration of the compound are, probably, associated with the complement depletion after its activation by carbogal particles or with disorders in the complement component synthesis by macrophages.

Animals↗
PubMed1992

The effect of systemic decomplementation with cobra venom factor on corneal complement levels in guinea pigs.

The authors examined the effect of systemic administration of cobra venom factor (CVF) on hemolytic complement levels in guinea pig sera and corneas. Guinea pigs received repeated intraperitoneal injections of CVF. Sera and corneas were obtained before and 1, 2, 5, 8, 10, 12, 16, and 20 d after the initial injection of CVF. Total hemolytic complement activity was measured by lysis of sheep erythrocytes sensitized with rabbit antibodies. There was a significant decrease in serum complement levels at days 1, 2, 5, 8, and 10 after the initial injection of CVF. After this, complement levels rose to levels that exceeded preinjection values. Complement levels in corneas also declined after CVF injections with a significant decrease at days 2, 5, 8, and 10 and a return to normal thereafter. Corneal complement depletion and restoration lagged behind serum. Moreover, the rate of complement depletion and restoration was greater for serum than cornea. Light microscopic examination of representative corneas at each time did not show local tissue changes during decomplementation. This is first study (to the authors' knowledge) to document corneal complement depletion by systemic administration of CVF. Low-to-absent corneal complement levels were present 2 d after the initial injection of CVF and persisted for 6 d. This model could be used to study the influence of complement on traumatic and immunologic injuries to the cornea.

Animals↗
PubMed1991

Inhibition of homologous complement by CD59 is mediated by a species-selective recognition conferred through binding to C8 within C5b-8 or C9 within C5b-9.

The capacity of the human complement regulatory protein CD59 to interact with terminal complement proteins in a species-selective manner was examined. When incorporated into chicken E, CD59 (purified from human E membranes) inhibited the cytolytic activity of the C5b-9 complex in a manner dependent on the species of origin of C8 and C9. Inhibition of C5b-9-mediated hemolysis was maximal when C8 and C9 were derived from human (hu) or baboon serum. By contrast, CD59 showed reduced activity when C8 and C9 were derived from dog or sheep serum, and no activity when C8 and C9 were derived from either rabbit or guinea pig (gp) serum. Similar specificity on the basis of the species of origin of C8 and C9 was also observed for CD59 endogenous to the human E membrane, using functionally blocking antibody against this cell surface protein to selectively abrogate its C5b-9-inhibitory activity. When E bearing human CD59 were exposed to C5b-8hu, CD59 was found to inhibit C5b-9-mediated lysis, regardless of the species of origin of C9, suggesting that the inhibitory function of CD59 can be mediated through recognition of species-specific domains expressed by human C8. Consistent with this interpretation, CD59 was found to bind to C5b-8hu but not to C5b67hu or C5b67huC8gp. Although CD59 failed to inhibit hemolysis mediated by C5b67huC8gpC9gp, its inhibitory function was observed for C5b67huC8gpC9hu, suggesting that, in addition to its interaction with C5b-8hu, CD59 also interacts in a species-selective manner with C9hu incorporated into C5b-9. Consistent with this interpretation, CD59 was found to bind both C5b67huC8gpC9hu and C5b-8huC9gp, but not C5b67huC8gpC9gp. Taken together, these data suggest that the capacity of CD59 to restrict the hemolytic activity of human serum complement involves a species-selective interaction of CD59, which involves binding to both the C8 and C9 components of the membrane attack complex. Although CD59 expresses selectivity for C8 and C9 of human origin, this "homologous restriction" is not absolute, and this human complement regulatory protein retains functional activity toward C8 and C9 of some nonprimate species.

Antigens, Differentiation↗
PubMed1991

[Complement fragments in patients with bronchial asthma].

In this study, we investigated the pharmacological reactions induced by ibudilast to the complement system with the aim of clarifying the functional relation of the complement system to allergic reactions and pathology in patients with bronchial asthma. Complement hemolytic activities (CH50 and ACH50), complement profile, anaphylatoxins (C3a and C5a) and complement fragments (Bb, iC3b and C4d) were measured in 20 patients with bronchial asthma. One of antiasthmatic activities induced by ibudilast was concluded to be brought about though inactivation of the alternative complement pathway working on type III allergic reaction. Ibudilast increased the complement fragment Bb in the patients' plasma with the fairly controlled bronchial asthma. This increase in circulating Bb was suspected to be a result of inactivation of intermediate complement complexes, for example C3b.Bb.P, because the amounts in plasma of C3 and C5 showed no changes, while those of factor, B, P, H and I were decreased by ibudilast administration in patients with fairly controlled bronchial asthma. This antiasthmatic ability of ibudilast was restrained in those patients whose peripheral leukocytopenia was advanced before ibudilast administration, and in those whom ibudilast did not provoke an increase in the plasma level of iC3b, or did not prevent the serum level of C5 from increasing. In those unfairly controlled cases, enough anaphylatoxins, especially C5a might be produced to make the margination of peripheral neutrophils to the lung and increase CR3 on neutrophils binding with iC3b.

Adult↗
PubMed1991

Complement in vitro inhibition by a low-sulfate chondroitin sulfate (matrix).

In this study, the ability of low-sulfate chondroitin sulfate (Matrix), a glycosaminoglycan that does not exhibit anticoagulant action, to inhibit the activation of complement has been evaluated. Two different in vitro tests were employed: lysis of mouse splenocytes sensitized with monoclonal antibodies and lysis of red blood cells sensitized using a rabbit antiserum towards those cells. In both tests, lyophilized rabbit complement was used as complement source. The low-sulfate chondroitin sulfate Matrix has been compared with a hypersulfated one (Arteparon). Both compounds share anticomplementary activity in vitro although potency appears to be related to the sulfate content of the chondroitin.

Animals↗
PubMed1991

Complement and monocytes are essential for provoking glomerular injury in passive Heymann nephritis in rats. Terminal complement components are not the sole mediators of proteinuria.

Complement but not polymorphonuclear granulocytes (PMN) causes glomerular injury in passive Heymann nephritis in rats. We have now identified monocytes as another important mediator in this model. Passive Heymann nephritis was induced in Wistar rats by intravenous injection of sheep anti-rat Fx1A antiserum. Four groups (all receiving anti-rat Fx1A antiserum) were studied: (a) rats given normal sheep globulin (nephritic controls), (b) rats given sheep anti-rat PMN globulin (PMN-depleted), (c) rats given sheep anti-rat monocyte globulin (monocyte-depleted), (d) rats injected with cobra venom factor (complement-depleted). In vitro specificity controls for anti-cell antisera were made by cytotoxicity tests and inhibition of phagocytosis. In vivo specificity controls were performed in heterologous Masugi nephritis (PMN-dependent) and accelerated Masugi nephritis (monocyte-dependent). Complement and monocyte depletion significantly delayed the onset of proteinuria (p less than 0.001 versus nephritic controls on day 5), PMN depletion had no significant effect. Monocyte infiltration was seen in control nephritic rats, but monocyte depletion prevented this influx. In the monocyte-depleted group, no differences in glomerular deposition of C3, C9, and C5b-9 were seen in comparison to the nephritic control rats. Serum C3 levels were comparable in groups a, b, and c, the complement system was biologically active in the monocyte depleted-group (c), and the amount of anti-Fx1A antibody bound was the same in all groups. This shows that, besides complement, monocytes are required for induction of renal damage in passive Heymann nephritis. The concept of a sole role for complement in glomerular immune injury involving subepithelial immune deposits should be reconsidered.

Animals↗
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↗