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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↗
PubMed1993

Splenic uptake of immune complexes in man is complement-dependent.

We have examined the effects of hereditary homozygous C2 deficiency on the processing of radiolabeled soluble immune complexes (IC). A patient with C2 deficiency was studied before and after treatment with fresh frozen plasma (FFP). Hepatitis B surface Ag (HBsAg):anti-HBsAg immune complexes were prepared in vitro using Ag radiolabeled with 123I, and injected intravenously. Dynamic and static gamma-scintigraphy was performed to delineate the sites and kinetics of complex clearance. The patient was initially studied when her C2 level and CH50 were zero, and again 1 wk later after treatment with 12 units of FFP, which normalized these parameters. Before treatment there was rapid uptake of complexes by the liver (t90% [time for 90% uptake] = 13.6 min) and rapid clearance from the circulation (t1/2 = 6.8 min). No splenic uptake was detected, and there was no binding of complexes to erythrocyte CR1. Between 30 and 60 min there was release of 11% of the tracer from the liver. In the second study, performed after normalization of classical pathway complement activity, the t1/2 of IC clearance increased to 9.8 min, and t90% was 27 min. Twenty percent of injected complexes now localized to the spleen, and there was no longer any release of complexes between 30 and 60 min. The kinetics of IC processing and the sites of uptake in this posttherapy study were closely similar to two normal subjects studied in parallel, with a maximum of 72% of injected complexes binding to erythrocytes. These observations indicate that the uptake of immune complexes in the spleen in humans is complement-dependent, and suggest that the observed predisposition to SLE in patients with complement deficiency may be related to abnormal processing of immune complexes.

Antigen-Antibody Complex↗
PubMedDate not supplied

[The anticomplement activity of Neisseria gonorrhoeae].

Bacteria of the species N. gonorrhoeae have anticomplementary activity whose absolute values exceed the level of this activity both in other representatives of the genus Neisseria and in microorganisms of other taxonomic groups found in the microbiocenosis of the reproductive tract. The specificity of the anticomplementary action of N. gonorrhoeae extracellular products with respect to individual components of the complement system, as well as their role in the formation of the state of seroresistance and in the determination of the effectiveness of the interaction of gonococci with neutrophilic phagocytes in the system of opsonic cooperation, have been characterized.

Blood Bactericidal Activity↗
PubMedDate not supplied

[The complement-activating action of modern x-ray contrast agents].

The study conducted proved that triombrast (dose dependently) > hexabrics > Ultravist > or = melitrast = omnipac in a concentration interval of 0.03-30.0 mg iodine/ml in vitro and in a dose interval of 0.5-2.0 g iodine/kg in vivo activate the complement system (CS) according to the alternative way in the blood of "sensitive" rats. The degree of CS activation by radiopaque agents (ROA) is significantly determined mathematically by their viscosity and relation of the number of iodine atoms to the number of ions or dissolved particles, and by their hydrophilic (for nonion CS) and osmotic (for ion monomeric CS) properties.

Animals↗
PubMedDate not supplied

[Hereditary angioedema: clinical and laboratory aspects of 7 cases].

Hereditary angioedema is caused by a defect in C1 inhibitor activity (C1INH). Its occurrence is rare and it is associated with an autosomal dominant mode of inheritance. We describe seven patients (4M:3F), age from 12 to 50 years old, who are affected by hereditary angioedema; four of them belong to the same family. The main clinical manifestations were: angioedema of face, hands and feet (6/7) and abdominal pain (2/7). No triggering factors were associated with symptoms in 4/7 patients and trauma (2/7) and menses (1/7) were reported in the other three ones. One patient was submitted to laparotomy for partial intestinal resection, before diagnosis. Laboratory complement analysis revealed the absence of hemolytic function of complement, reduced C4 (6/7) and low C1INH levels. All patients received Danazol (100 mg/day) with clinical control. Hereditary angioedema has to be considered in the differential diagnosis of angioedema, since an early diagnosis of this immunodeficiency, leading to specific treatment in order to decrease the complications.

Adult↗
PubMed1998

[Threshold mechanism of the control of cascade proteolysis].

The immune lysis rate of erythrocytes vs. the concentration of particular complement components was studied. It was found that in the presence of component C1 (but not C3) and factors B and D, the cells undergo lysis after the concentration of these compounds exceeds a "threshold" value. The threshold molar concentrations of factors D and B exceeded 5- and 20-fold, respectively, that of component C1. The multiplicity and different capacities of the thresholds allow the fragmentary activation of cascade proteolysis at stretches between neighboring thresholds without the total realization of the final effect of the system (cell lysis, clot formation, etc.). The resulting peptideby-products (bypass peptides) may possess their own biological activity. It is the generation of various bioregulators that appears to be the main function of the cascade proteolytic systems functioning in the subthreshold regime.

Animals↗
PubMed1985

Hemolytic plate assay for quantification of active human complement component C3 using methylamine-treated plasma as complement source.

A hemolytic plate assay specific for active human complement component C3 is described. The method is well suited for tracing active C3 during preparative purification or for screening of plasma samples. The assay is based on activation of the alternative pathway of complement by unmodified rabbit erythrocytes. Plasma treated with methylamine supplies the essential complement components other than C3. The lytic reaction is complete in 5 h at 37 degrees C and is unchanged by incubation overnight. The dose-response curve, i.e., lysis diameter versus logarithm of C3 concentration, is linear within 0.1-10 times normal plasma concentrations of C3. The standard deviation is below 10%. The hemolytic agarose plates are easy and inexpensive to prepare, and they can be stored at 4 degrees C for 2 weeks before use. This paper describes the optimal conditions of the assay and proves its specificity. Its use in C3 preparation and plasma screening for C3 is discussed.

Animals↗
PubMed1989

A hemolytic assay for the measurement of equine complement.

A hemolytic assay was developed for the measurement of functional equine complement activity. The assay utilizes antibody sensitized chicken erythrocytes as the target cell and was specific for classical pathway (antibody dependent) complement activity. The assay was found to be reproducible and more sensitive than previous reports using other species of target cells. Total serum complement (CH50) values were determined for five mares and their foals and followed over a period of 3 months.

Animals↗
PubMed1992

The effects of complement depletion on corneal inflammation in rats.

There are indications that complement activation may be involved in inflammatory processes of the cornea. To investigate the role of the complement system in experimental keratitis, rats were depleted of their plasma complement by treatment with cobra venom factor (CVF). intraperitoneal injection of CVF resulted in undetectable complement serum activity for 6 days when measured by a hemolytic assay. The corneal inflammatory response, induced by a single intracorneal injection of heterologous serum into nonsensitized CVF-treated rats, was suppressed significantly. The onset of the clinical symptoms of keratitis was delayed, and the severity was reduced. In addition, analysis of the serum antibody titers showed impaired antibody synthesis in the CVF-treated group. When keratitis was induced by an intracorneal antigen challenge in sensitized rats, no difference was observed when comparing the clinical signs of keratitis of CVF-treated animals with sham-treated animals. In addition, CVF treatment did not alter the course of lipopolysaccharide (LPS)-induced corneal inflammation. These findings suggest that the role of plasma complement activation in antigen- and LPS-induced keratitis appears to be limited. The implications for the immunopathologic mechanisms underlying keratitis are discussed.

Animals↗