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PubMed1985

Leishmania amastigotes: resistance to complement-mediated lysis is not due to a failure to fix C3.

Amastigote forms of Leishmania major are sensitive to lysis by fresh serum, whereas those of L. donovani are resistant. To understand the basis for this resistance we have examined the interaction of complement with amastigotes of seven strains of leishmania. Complement activation was determined by measuring the ability of amastigotes to consume complement from normal serum and by identifying parasite surface-bound C3. All of the strains that were tested activated complement, including both those that are resistant and those that are susceptible to inactivation by fresh serum. Complement consumption by amastigotes was measured as a decrease in the ACH 50 titers of serum exposed to parasites. L. major, L. donovani, and L. mexicana mexicana (strain 1VLM) amastigotes decrease titers by 35.7, 33.5, and 40.3%, respectively. The binding of C3 to amastigotes was judged qualitatively by immunofluorescence and quantitatively by a C3 radiobinding assay. L. major amastigotes bind an average of 6.6 X 10(4) molecules of C3 per parasite. L. mexicana amazonensis, L. mexicana mexicana, and L. donovani bind an average of 3.9 X 10(4), 5.9 X 10(4), and 3.7 X 10(4) molecules, respectively. In all cases, C3 binding is the result of alternative pathway activation requiring Mg++ but not Ca++. Amastigotes of the disseminating strains of leishmania represent the first example of a group of protozoa that activate early complement components leading to fixation of C3, but that are resistant to inactivation by complement.

Adult↗
PubMed1985

Inhaled asbestos activates a complement-dependent chemoattractant for macrophages.

Pulmonary macrophages migrate to the sites where inhaled chrysotile asbestos fibers initially are deposited (i.e., surfaces of alveolar duct bifurcations). These macrophages have been shown to form a major component of an early asbestos-induced interstitial lesion in rats. In this report, we describe a potential mechanism by which macrophages are attached to these sites of fiber deposition. Chrysotile asbestos fibers used in vitro activate complement proteins in peripheral blood serum and in lavaged cell-free lung proteins. After brief inhalation of chrysotile asbestos, fluids lavaged from the lungs of exposed rats contain substantial chemotactic activity for macrophages compared to fluids from sham-exposed animals (p less than 0.01). We hypothesize that this chemotactic activity is derived from complement activated by inhaled asbestos on alveolar surfaces. This contention is supported by the following observations. Production of chemotactic activity by asbestos in vitro in serum or in lavaged lung fluids was blocked by complement inhibitors. Fractionation, by molecular sieve chromatography, of serum proteins and concentrated proteins lavaged from the lungs of asbestos-exposed rats showed that chemotactic activity was detected in the 14,000- to 18,000-dalton range. This fractionation profile is similar to C5a, the chemotactic product of complement activation. Rats treated with cobra venom factor to deplete circulating complement as well as complement-deficient mice demonstrated significantly depressed macrophage accumulation at sites of asbestos deposition. Pulmonary macrophages are the cells that form the initial inflammatory response to asbestos inhalation. Our findings support the hypothesis that asbestos fibers, and possibly other inhaled particulates, activate complement-derived chemotactic activity on alveolar surfaces. Consequently, macrophages are attracted to the alveolar duct bifurcations where inhaled asbestos fibers are deposited, and this is where the initial lesion of asbestosis is manifested.

Animals↗
PubMedDate not supplied

Complement activation and cyto-immunological alterations of the respiratory mucosa.

The action of activated complement on the upper respiratory tract was studied using the registration of ciliary beating and the transmission and scanning electron microscopy of ciliated cell lesions. The alternative pathway of activation was done using (1) non-specific activators, i. e. zymosan, dextran sulfate and polymerised sIgA, and (2) specific activators, i. e. "Ag-sIgA" immune complexes on normal mucosa and contact between an antigen and the tracheal mucosa of an immunized animal. In all cases, a quick alteration of the ciliary beating rythm was registered as well as more or less extensive cytological destruction. Such results were obtained with or without adjunction of complement; this suggested the existence of complement locally. A new method to demonstrate the occurrence of complement was developed, and the results showed that complement was present in the trachea. The above results were corroborated (1) by EDTA inhibition of the two complement pathways which prevented stopping of the ciliary beating and eliminated most of the cytological lesions, whilst EGTA left the alternative pathway operative with consequent alterations, and (2) by using C6-deficient rabbits in which no alterations were found. This study demonstrated that under certain conditions, local sIgA may activate the complement, and this fact explains many aspects of these immunological reactions of the respiratory epithelium.

Animals↗
PubMed1981

Activated factor B (Bb) of the alternative pathway of complement activation cleaves and activates plasminogen.

Activated Factor B (Bb), the central serine esterase of the alternative pathway of complement activation, exhibits restricted substrate specificity in the complement system for C3 and C5. The results presented here indicate that Bb can cleave and activate plasminogen in an experimental system containing purified plasminogen and Bb; complement cellular intermediate bearing the Bb-enzyme; or cobra venom factor-stabilized Bb-enzyme (CVF,Bb). Cleavage of plasminogen by Factor Bb generated 2 disulfide-linked polypeptides with apparent m.w. of 64,000 and 25,000 to 32,000 (SDS-PAGE). Complement cellular intermediates containing the C3b, Bb-enzyme cleave 40 to 80% of 4.5 micrograms of 125I-labeled plasminogen during 30 min of incubation at 37 degrees C; native Factor B was inactive; and anti-Factor Blg inhibited by 100% the plasminogen cleavage mediated by complement cellular intermediates bearing the Bb-enzyme. Fibrinolytic activity was detected in plasminogen activator (PA) assays when purified plasminogen and 125I-labeled fibrin tubes were incubated with Bb, CVF, Bb, or complement cellular intermediates bearing the C3b,Bb-enzyme: 10 micrograms Bb released 40 to 65% of the 125I-fibrin released by 5 micrograms urokinase in 4 hr at 37 degrees C. Plasminogen activator activity of the C3b,Bb-enzyme was found to be regulated in serum. At dilutions of NHS 1:50, the PA-activity of 1.6 micrograms Bb was 100% inhibited, and at a 1:250 dilution, 50% inhibition was observed. This report describes a novel activity for the Bb-enzyme, which constitutes the C3/C5-convertase of the alternative pathway of complement activation.

Complement Activation↗
PubMed1981

Biosynthesis of complement components.

Many of the serum complement components are synthesized primarily in the liver but extrahepatic synthesis in mononuclear phagocytes has been noted. This local production of complement, particularly at sites of inflammation, may be of importance in host defenses and immunopathological reactions. Recent studies of complement biosynthesis in vitro have revealed some of the genetic and microenvironmental factors that affect the rates of complement synthesis, posttranslational modification, and secretion of these proteins. The third, fourth, and fifth complement components are synthesized as single chain, procomplement proteins that require proteolytic cleavage to generate the native C4 protein is mediated by a plasmin-like enzyme. These studies, plus the most recent developments in analysis of the complement genes at a molecular level, will provide more complete understanding the mechanisms of regulation of complement production.

Animals↗
PubMed1995

Complement and IgG subclasses in agammaglobulinemic patients.

Complement and IgG subclass analysis was performed in six agammaglobulinemic patients suffering from recurrent bacterial infections. Complement analysis included functional activity of the classical (CH50) and the alternative pathway (APH50) of complement, the complement proteins C3, C4, factor B, the regulators C1-inhibitor, factors H and I as well as the C3-derived split product C3dg/C3d. Plasma concentrations of total IgG ranged between < 0.01 and 297 mg/dl. IgM and IgA were almost undetectable. Levels of all IgG subclasses, which in most cases were measurable only by sensitive ELISA, were markedly reduced in all patients. A pronounced activation of the complement system was observed in all patients as revealed by reduced titers of hemolytic function and elevated levels of C3dg/C3d. Despite the fact that complement activation by itself was the major reason for decreased C4 levels, from depressed plasma concentrations of the common allotypic variants C4A and C4B, a heterozygous C4 deficiency could not be excluded in 2/6 patients. Our data clearly show that, by application of sensitive analytical methods, agammaglobulinemic patients vary considerably in their ability to synthesize immunoglobulins. This may, at least in part, explain the heterogeneous pattern of clinical symptoms. The increased susceptibility of agammaglobulinemic patients to bacterial infections is reflected by a highly activated, and thereby depleted complement system.

Adolescent↗
PubMed1993

Inhibitory effect of FUT-175 on complement activation and its application for glomerulonephritis with hypocomplementemia.

FUT-175 (6-amidino-2-naphthyl p-guanidinobenzoate dimethane-sulphonate), a potent serine protease inhibitor, has been reported to inhibit complement activity in vitro, and especially the classical complement pathway effectively. In the present study, we examined the inhibitory effect of FUT-175 on the classical complement pathway components by hemolytic assay using purified human complement components. As a result, 50% inhibition of the C1 protease activity for classical C3 convertase formation and for C2 was obtained with 3.0 x 10(-8) M and 7.0 x 10(-8) M of FUT-175, respectively. FUT-175 did not inhibit the C2 protease activity at all. We then administered FUT-175 to 5 glomerulonephritic patients with hypocomplementemia and proteinuria in order to assess the clinical effectiveness of this drug. When FUT-175 was administered intravenously and continuously at a rate of 0.1 to 0.2 mg/kg/hr for 2 weeks, the urinary protein excretion decreased significantly from 2.9 +/- 0.8 to 1.4 +/- 0.5 g/day (P < 0.025). In these patients, some of the serum complement markers (serum C3, C4 level and the hemolytic activity via the classical complement pathway (CH50)) were increased after FUT-175 administration. The above findings suggests that FUT-175 can exert beneficial effects on glomerulonephritis with hypocomplementemia by inhibiting complement activation.

Adult↗
PubMed1996

Human carcinomas variably express the complement inhibitory proteins CD46 (membrane cofactor protein), CD55 (decay-accelerating factor), and CD59 (protectin).

Normal human tissues express membrane-associated complement inhibitory proteins that protect these tissues from damage by autologous complement. To determine whether neoplasms also express these proteins, we examined the distribution of the complement inhibitors decay-accelerating factor (DAF), CD59 (protectin), and membrane cofactor protein in frozen samples of human breast, colon, kidney, and lung carcinomas and in adjacent non-neoplastic tissues, using immunohistochemistry. All samples were also studied for deposition of C3 fragments and activated C5b-9. Differences between normal tissues and the corresponding neoplasms were often observed, with loss or gain of expression of one or more inhibitors. Ductal carcinomas of the breast showed the most variation in phenotype; some tumors expressed only one inhibitor while others expressed different combinations of two or three inhibitors. Colon carcinomas, by contrast, stained intensely for all inhibitors. Renal cell carcinomas had weak to moderate expression of one to three inhibitors, generally DAF and CD59, whereas non-small cell carcinomas of the lung usually expressed CD59 and membrane cofactor protein with variable DAF immunoreactivity. The two small cell carcinomas of the lung showed little or no staining for any inhibitor. Activated C5b-9 deposition was seen adjacent to tumor nests in a minority of carcinomas and showed no correlation with complement inhibitor expression. C3 fragment deposition was minimal. Our results demonstrate that most carcinomas, with the exception of small cell carcinomas of the lung, do express one or more complement inhibitors at a level likely to inhibit complement-mediated cellular damage. Unexpectedly, large quantities of DAF and CD59 were often observed in tumor stroma, with only limited deposition in normal connective tissue. This suggests that carcinomas may supplement the activity of membrane-associated complement inhibitors by release of soluble forms of DAF and CD59 into the surrounding extracellular matrix.

Antigens, CD↗
PubMed1997

Evidence for intrathecal synthesis of alternative pathway complement activation proteins in experimental meningitis.

Complement has been shown to contribute to intrathecal inflammation in bacterial meningitis. However, the cellular source of complement in the infected central nervous system has not been determined. In this study, we analyzed protein and mRNA expression of two alternative pathway complement activation proteins, C3 and factor B, in the brains of mice with Listeria monocytogenes meningitis. Complement protein levels were found elevated in the cerebrospinal fluid of infected mice, compared with mock-infected animals. In the course of the disease, enhanced C3 and factor B mRNA expression was detected on pyramidal neurons and Purkinje cells within 6 hours, peaking at 12 hours and then gradually decreasing by 72 hours after infection. In addition, leukocytes infiltrating the subarachnoid space, within 12 to 24 hours, expressed mRNA for C3 and factor B. The cellular infiltration increased dramatically up to 72 hours. Intraperitoneal injection of tumor necrosis factor (TNF)-alpha up-regulated C3 and factor B mRNA expression on neurons in normal mice, suggesting that TNF-alpha may represent one cytokine regulating complement expression in this model of bacterial meningitis. However, additional mediators may be involved in regulation of intrathecal complement expression, as infected mice deficient of TNF/lymphotoxin-alpha genes did not demonstrate attenuated complement expression in the brain.

Animals↗
PubMed1998

[Methods of in vitro assessment of the degree of complement activation by the classical pathway].

A sensitive a simple method is proposed for assessing the complement activation degree by the monospecific classical route. The alternative pathway of the complement activation proposed by Adachi et al. in 1990 is taken account of. The specific features of the proposed method are 1) use of commercial dry complement of guinea pigs with the regulatory protein defect needed for the alternative pathway of complement activation; 2) absence of EGTA in GVB and presence of Ca2+; 3) use of sensitized sheep red blood cells as the target cells. These conditions prevent the alternative pathway of complement activation and permit only the classical pathway. Effects of some drugs on the classical pathway of complement activation by the new method and on Adachi's alternative method are investigated. Estradurin and fosfestrol affect the complement activation by both pathways.

Animals↗
PubMed1998

The semisynthetic polysaccharide pentosan polysulfate prevents complement-mediated myocardial injury in the rabbit perfused heart.

Pentosan polysulfate (PPS) is a highly sulfated semisynthetic polysaccharide possessing a higher negative charge density and degree of sulfation than heparin. Like other glycosaminoglycans, the structural and chemical properties of PPS promote binding of the drug to the endothelium. Glycosaminoglycans, including heparin, inhibit complement activation independent of an action on the coagulation system. This ability provides a compelling argument for the implementation of this class of compounds in experimental models of cellular injury mediated by complement. The objective of this study was to examine whether PPS could reduce myocardial injury resulting from activation of the complement system. We used the rabbit isolated heart perfused with 4% normal human plasma as a source of complement. Hemodynamic variables were obtained before addition of PPS (0.03 01 mg/ml) and every 10 min after the addition of human plasma. Compared with vehicle-treated hearts, left ventricular end-diastolic pressure was improved at the conclusion of the 60-min protocol in hearts treated with PPS (58.9 +/- 13.6 vs. 15. 2 +/- 4.8 mm Hg). Further evidence as to the protective effects of PPS was demonstrated by decreased creatine kinase release compared with vehicle (86.5 +/- 28.5 U/l vs. 631.0 +/- 124.8 U/l). An enzyme-linked immunosorbent assay for the presence of the membrane attack complex in lymph and tissue samples demonstrated decreased membrane attack complex formation in PPS-treated hearts, which suggests inhibition of complement activation. This conclusion was supported further by the ability of PPS to inhibit complement-mediated red blood cell lysis in vitro. The results of this study indicate that PPS can reduce tissue injury and preserve organ function that otherwise would be compromised during activation of the human complement cascade.

Animals↗
PubMed1998

Glial cell responses, complement, and clusterin in the central nervous system following dorsal root transection.

We have examined the glial cell response, the possible expression of compounds associated with the complement cascade, including the putative complement inhibitor clusterin, and their cellular association during Wallerian degeneration in the central nervous system. Examination of the proliferation pattern revealed an overall greater mitotic activity after rhizotomy, an exclusive involvement of microglia in this proliferation after peripheral nerve injury, but, in addition, a small fraction of proliferating astrocytes after rhizotomy. Immunostaining with the phagocytic cell marker ED1 gradually became very prominent after rhizotomy, possibly reflecting a response to the extensive nerve fiber disintegration. Lumbar dorsal rhizotomy did not induce endogenous immunoglobulin G (IgG) deposition or complement expression in the spinal cord dorsal horn, dorsal funiculus, or gracile nucleus. This is in marked contrast to the situation after peripheral nerve injury, which appears to activate the entire complement cascade in the vicinity of the central sensory processes. Clusterin, a multifunctional protein with complement inhibitory effects, was markedly upregulated in the dorsal funiculus in astrocytes. In addition, there was an intense induction of clusterin expression in the degenerating white matter in oligodendrocytes, possibly reflecting a degeneration process in these cells. The findings suggest that 1) complement expression by microglial cells is intimately associated with IgG deposition; 2) axotomized neuronal perikarya, but not degenerating central fibers, undergo changes which induce such deposition; and 3) clusterin is not related to complement expression following neuronal injury but participates in regulating the state of oligodendrocytes during Wallerian degeneration.

Animals↗
PubMed1984

Mechanisms of leukocyte regulation by complement-derived factors.

Progress over the past five years has drawn attention to the fact that the anaplylatoxins are important factors in both leukocyte activation and regulation events. The C5 anaphylatoxin has been proposed to play major role in leukocyte aggregation and adherence phenomenon. Influences of C5a on the leukocyte may lead to clinical manifestations such as respiratory distress syndrome after trauma or postpump syndrome after cardiopulmonary bypass, both effects derived from leukocyte sequestration. Many other clinical conditions involving repeated transient sequestration of leukocytes, particularly in the pulmonary vasculature, may eventually be recognized as a complication of systemic complement activation. Dramatic pathologic changes observed in the lungs of animals exposed to either C3a or C5a emphasizes the potential damage that these factors may exert via cellular activation mechanisms (Huey et al., 1983). More recent evidence that the anaphylatoxins are potent immunoregulatory factors under in vitro conditions suggests a physiologic role for these humoral factors in nonspecific modulation of the immune response. It is an attractive hypothesis to suggest that once activated, complement is capable of relaying information to the cellular immune system via the anaphylatoxins. Other components of the complement system have long been known to exert regulatory influences on the immune system, and perhaps molecular description of such entities as the C3d-K fragment will serve to unravel this seemingly more complex effector system. In any case, as our understanding of both the chemical and biologic nature of factors derived from blood complement components advances, it has become apparent that a major function of complement may be to modulate the immune response. We have already demonstrated that these factors are selective both for cell type and for eliciting a variety of cellular responses. From this, one can infer that manipulation of the cellular events will eventually be possible. Hence a therapeutic value may be realized once involvement of these complement factors under in vivo conditions is better characterized.

Anaphylatoxins↗
PubMed1992

Cold-dependent activation of complement: recognition, assessment, and mechanism.

Cold-dependent activation of complement (CDAC) is a phenomenon characterized by low hemolytic complement activity in chilled serum. Complement component levels are normal when measured immunologically, and there is normal hemolytic activity in EDTA plasma or serum maintained at 37 degrees C. Little attention has been paid to CDAC except in Japan, and current unfamiliarity with it, even by clinical immunologists, can lead to confusion and unnecessary laboratory tests. A 66-year-old patient with a complex medical history is described whose complement tests showed abnormalities characteristic of CDAC. Evidence for classical complement pathway activation in the cold was obtained by CH50 measurements, by hemolytic C4 determinations, by C4a, C3a, and C4d generation, and by quantitating C1s-C1r-(C1 inhibitor)2 complexes. A good correlation was observed among these parameters. Cryoprecipitates were absent. CDAC activity has persisted for over 5 years and is greater at 13 than at 4 degrees C. Activation is ablated by heating at 56 degrees C and restored by the addition of C1 to the heated serum. Adsorption by streptococcal protein G-Sepharose and precipitation by 2.5% polyethylene glycol support the hypothesis that CDAC is caused by aggregated IgG. The CDAC factor(s) also induces complement activation in normal serum but has not interfered with Raji cell or C1q binding tests or with FACS analysis. More limited studies of a second individual experiencing CDAC yielded similar results.

Adult↗
PubMed1985

Suppression of mouse complement activity by contaminants of technical grade pentachlorophenol.

Pentachlorophenol (PCP) is an antimicrobial agent used chiefly for the preservation of wood. Subchronic oral exposure (14 days) to Technical Grade PCP significantly inhibited the functional activity of female B6C3F1 mouse complement when measured in a microtiter hemolytic assay. When evaluated one day following the final exposure the highest administered dose (100 mg/kg) significantly suppressed the Classical complement pathway, the Spontaneous C1 autoactivation pathway, the Alternate pathway and the level of complement component, C3. Reconstitution studies using C5-deficient serum also demonstrated deleterious effects on this complement component. The Classical pathway was the most sensitive to Technical Grade PCP effects. Animals treated with 100 mg/kg Technical Grade PCP had CH 50 levels 30% of vehicle controls. Animals treated for 14 days and allowed a 15 day recovery period had CH 50 values 36% of control and animals which recovered for 30 days had only 52% of the complement activity of control animals. C3 recovery studies also demonstrated continued suppression on days 15 and 30 post-final exposure. Doses of 10 and 30 mg/kg did not produce the marked effects observed with the highest dose; however, a dose-dependent trend was observed for all responses. Animals treated with 100 mg/kg of EC-7, a PCP preparation with reduced amounts of contaminating dioxins and dibenzofurans, did not demonstrate detrimental effects on the complement system.

Animals↗
PubMed1979

Complement in tears from normal humans.

Tears from ten normal persons were used in hemolytic assays to test for activity of total hemolytic complement (tested in all ten subjects), activities of each of the nine complement components (tested in two subjects), and activity of the alternate pathway (tested in two subjects). A modified radial-immunodiffusion method was used to confirm the presence of C3 and C4 complement proteins in the tear samples from all ten subjects. Factor B protein was detected in tears from two of four normal subjects tested. In dilutions up to 1:4, hemolytic activity was observed in tears from five of the ten subjects. Samples from the remaining five subjects had CH50 activity at dilutions up to 1:2. In control tests, human serum had CH50 activity at 1:32. No lysis occurred in Veronal-buffered saline or in serum and tears heated to 56 degrees C for 30 minutes. Complement proteins C3 through C9 displayed hemolytic activity in tears from each of two subjects tested for complement components. The classic and alternate complement pathways in tears can be included among the defense mechanisms of the ocular surfaces.

Complement C3↗
PubMed1986

Compartmental distribution of complement activation products in artificial kidneys.

The compartmental distribution of the human anaphylatoxins C3a and C5a has been defined during simulated hemodialysis performed with various types of hemodialyzers. New cuprophan hollow fiber dialyzers were found to activate human complement very readily in vitro, while re-used cuprophan dialyzers displayed only modest complement activating potential. The C3a and C5a antigens, formed as a result of complement activation in these dialyzers, accumulated predominantly in the blood path and were not adsorbed extensively on the membrane surface or transported into the dialysate compartment. Cellulose acetate membranes also produced complement activation in vitro, but to a lesser degree than new cuprophan hollow fibers. However, these membranes exhibited a significant capacity to bind the anaphylatoxins to their surface. Polyacrylonitrile membranes appeared to be unique in that they not only failed to activate complement significantly, but they rapidly adsorbed large quantities of C3a and C5a. These findings demonstrate that hemodialysis membranes may differ with regard to their complement activating potential as well as their ability to remove circulating anaphylatoxins from the blood path. Clinical measurements of anaphylatoxin production during hemodialysis reflect these dynamic events.

Complement Activation↗
PubMed2001

Streptococcal inhibitor of complement (SIC) inhibits the membrane attack complex by preventing uptake of C567 onto cell membranes.

Streptococcal inhibitor of complement (SIC) was first described in 1996 as a putative inhibitor of the membrane attack complex of complement (MAC). SIC is a 31 000 MW protein secreted in large quantities by the virulent Streptococcus pyogenes strains M1 and M57, and is encoded by a gene which is extremely variable. In order to study further the interactions of SIC with the MAC, we have made a recombinant form of SIC (rSIC) in Escherichia coli and purified native M1 SIC which was used to raise a polyclonal antibody. SIC prevented reactive lysis of guinea pig erythrocytes by the MAC at a stage prior to C5b67 complexes binding to cell membranes, presumably by blocking the transiently expressed membrane insertion site on C7. The ability of SIC and clusterin (another putative fluid phase complement inhibitor) to inhibit complement lysis was compared, and found to be equally efficient. In parallel, by enzyme-linked immunosorbent assay both SIC and rSIC bound strongly to C5b67 and C5b678 complexes and to a lesser extent C5b-9, but only weakly to individual complement components. The implications of these data for virulence of SIC-positive streptococci are discussed, in light of the fact that Gram-positive organisms are already protected against complement lysis by the presence of their peptidoglycan cell walls. We speculate that MAC inhibition may not be the sole function of SIC.

Bacterial Proteins↗