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PubMed1985

[Comparative immunopathologic study of oral aphthae, non-involved mucosa from aphthae patients, healthy mucosa and trauma-induced ulcers].

The presence of IgG, IgA, IgM, C1q, C3c, fibrinogen and properdin has been studied using direct immunofluorescence technique. The same study has been performed in clinically normal mucosa of patients with aphthous ulcers, normal mucosa of healthy volunteers and traumatically induced ulcers. We have also studied the possible presence of reactive serous immunoglobulins with normal mucosa by indirect immunofluorescence. Our findings do not support previous studies which claimed the presence of vasculitis induced by the presence of immunoreactants in the vessel walls.

Adolescent↗
PubMed1979

Complement activation by pneumococci associated with acute otitis media.

Pneumococci (types, I, III, VI, XIV, XVIII, XIX and XXIII) associated with acute otitis media were shown to activate complement in normal human serum by the classical as well as by the alternative pathway. In serum incubated with pneumococci classical pathway activation was demonstrated by decreased C4 values and the appearance of C1r-C1s-C1 IA complexes. Pneumococci caused C3 conversion in C2-deficient serum and in serum chelated with Mg++ EGTA showing activation of the alternative pathway without participation of the C42 convertase. Complement activation was more efficient when both pathways were intact. This was evident from a more pronounced C3 conversion and a greater reduction of the values for properdin and factor B in non-chelated serum as compared to Mg++ EGTA chelated serum.

Acute Disease↗
PubMed1985

Experimental Bacteroides fragilis bacteremia in a primate model: evidence that Bacteroides fragilis does not promote the septic shock syndrome.

Experimental Bacteroides fragilis bacteremia was studied in subhuman primates. Following intravenous infusion of viable B. fragilis there was an exponential clearance of organisms from the bloodstream. The major clearance organ was the liver, which accumulated 68.2% of the total inoculum. The most efficient clearance was exhibited by the spleen, with uptake of 1.16% gm tissue. Hemodynamic studies revealed no significant changes in heart rate, mean arterial pressure, or cardiac output following B. fragilis infusion. Complement activity as measured by CH50, alternative pathway hemolytic activity, granulocyte aggregometry, C4, C3, properdin, and Factor B levels were similarly unaffected by infusion of B. fragilis. In contrast, profound hemodynamic changes and a consistent decrease in complement activity was noted after challenge with S. minnesota. The results of this study suggest that B. fragilis bacteremia has a minor role in producing the acute hemodynamic changes associated with the septic shock syndrome.

Animals↗
PubMed1979

Action of the C3b-inactivator on the cell-bound C3b.

The action of C3bINA and beta 1H on cell-bound C3b is described in this paper. The alpha-polypeptide of C3b that binds covalently to cell surfaces is cleaved by the C3bINA and beta 1H into two fragments: one of 60,000 (C3b alpha-60) and another of 40,000 (C3b alpha-40) daltons. The beta-chain of C3b is unaffected by the C3bINA and beta 1H. The three polypeptides, C3b alpha-60, C3b alpha-40, and C3 beta, are held together as a single unit by disulfide bonds. This unit, referred to as C3b' is covalently bound to cell surfaces via the C3b alpha-60 polypeptide. The conversion of C3b to C3b' by C3bINA and beta 1H abolishes the ability of the C3b-bearing cells to adhere to human erythrocytes as well as the ability to form, on the cell surface, the B, D, and properdin-dependent amplification C3-convertase. However, the agglutinability of the cells with either anti-C3c or anti-C3d is not affected. Treatment of the C3b'-bearing cells with trypsin releases fragments of C3b' into solution, leaving a polypeptide of 32,000 daltons covalently linked to the membrane. Since the trypsinized cells are agglutinable by anti-C3d but not by anti-C3c, the 32,000 dalton polypeptide appears to correspond antigenically to C3d.

Animals↗
PubMed1979

Further characterization of "promptly" and "delayed" human serum-sensitive strains of Serratia marcescens.

The kinetics of the bactericidal activity of 80 vol% of fresh human serum against representative 'delayed serum-sensitive' (DSS) and 'promptly serum-sensitive' (PSS) strains of Serratia marcescens were further examined with regard to various chemical and absorption procedures known to affect various components of the alternative and classical pathways of human complement activation. Inulin treatment of fresh human serum failed to diminish serum bactericidal activity against DSS and PSS assay strains. Fresh human serum that had been depleted of properdin (factor P) through absorption with zymosan, was as active as control serum against DSS strains of S. marcescens; however, PSS strains were killed in a 'delayed' fashion. Human serum that had been heat-inactivated at 50 degrees C for minutes (depletion of factor B), no longer killed DSS strains, whereas PSS strains of S. marcescens and the PSS control strain Escherichia coli C were killed in a slightly delayed fashion. Hydrazine-hydrate treatment (inactivation of C3 of the complement system) and exposure of fresh human serum to dithiothreitol completely abolished serum bactericidal activity. Bentonite-absorbed fresh human serum no longer killed DSS strains of S. marcescens; some PSS strains of S. marcescens were killed in a delayed manner, whereas control strain E. coli C was as PSS as before. Addition of Seitz-filtered fresh human serum, that lacked beta-lysin and was deficient in lysozyme, to bentonite-absorbed human serum restored bactericidal activity against DSS and PSS strains of S. marcescens; addition to heat-inactivated or Seitz-filtered, heat-inactivated human serum failed to do so. Therefore, bentonite absorption removed to a heat-labile component from fresh human serum clearly different from beta-lysin and lysozyme. Furthermore, human serum beta-lysin and lysozyme were not required for serum-mediated killing of S. marcescens strains of either serum susceptibility category.

Absorption↗
PubMed1979

Substrate modulation as a control mechanism in the activation of plasma multienzyme systems.

Since plasma is a homogenous fluid its biochemical systems need special control mechanisms to prevent their unlimited and continuous activity. In general, enzymic activity is not preformed but generated by trigger processes. Activation is then enhanced by cascade reactions. It can be controlled by enzyme inhibitors, by enzymes which destroy co-factors, or by spontaneous decay or enzyme complexes involved in the system. In addition, in some reactions of the complement and Hageman factor-dependent systems the necessity of substrate modulation controls the extent of activation. Thus, factor B of the properdin system is activatable by factor D only when bound to the activated third component of complement, and C3b fragment; similarly C2 is activated and forms the C3 converting complex, C42, only when bound to C4b prior to its cleavage by C1; C5 can be activated by either of the two convertases only when bound to surface-fixed C3b; and the mutural activation of Hageman factor and pre-kallikrein on surfaces proceeds efficiently only when HMW-kininogen is present which complexes with pre-kallikrein and possibly with Hageman factor.

Complement C3↗
PubMed1979

Effect of a streptococcal preparation on the complement system.

Streptococcal preparation OK-432 (Picibanil), clinically being used as an immunopotentiator, has been shown to activate the complement system either through the classical or the alternative pathway in vitro [15]. In this experiment, OK-432 was found to increase serum complement level in guinea pigs, and in human without malignancy, when investigated by hemolytic assay using sensitized sheep erythrocytes (EA) for the classical pathway activity and unsensitized rabbit erythrocytes (RaE) for the alternative pathway activity. Assay of complement components revealed a significant increase in C3, but decrease in Clq, while no specific tendency was observed in C4, C5, C9, properdin, C3 activator and Cl-inhibitor. These evidences suggested that OK-432 might potentiate immune response of the host by elevating serum complement level, in addition to activate the complement system.

Aged↗
PubMed1976

Dissociation of anticomplementary and adjuvant properties of proteins derived from cobra venom.

The ability of preparations of cobra factor (CoF) to convert C3 via the properdin pathway (anticomplementary activity) has been demonstrated to be unrelated to its ascribed ability to convert a tolerogenic signal into an immunogenic stimulus (adjuvant activity). It has been shown that CoF preparations which have become inactive with regard to anticomplementary activity still retain full adjuvant properties. Further, when both activities are present in preparations of CoF, they can be separated by gel filtration chromatography into a fraction with approximate molecular weight 150,000 which contains anticomplementary activity and a fraction with approximate molecular weight 20,000, which contains adjuvant properties.

Adjuvants, Immunologic↗
PubMed1978

Chronic idiopathic thrombocytopenic purpura. A familial immunodeficiency syndrome?

We studied three children with chronic idiopathic thrombocytopenic purpura (ITP) and their immediate families. All three patients and 10/13 family members manifested at least one immunologic defect, eg, decreased numbers of T lymphocytes (1/3, 5/13), diminished in vitro response to phytohemagglutinin (2/3, 6/13), dysgammaglobulinemia (2/3, 4/13), altered autoantibodies (1/3, 5/13), and decreased serum properdin levels (3/3, 2/13). In addition, one parent and two asymptomatic siblings of two of the propositi had shortened platelet life spans with normal platelet counts. The HLA antigens A3 and B7 were identified in all three families. There also appeared to be an association between a familial haplotype and the immunologic defects. Chronic ITP appears to occur in families with underlying immunologic defects, which are genetically related.

Adolescent↗
PubMed1982

Adrenergic receptors on monocytes modulate complement component synthesis.

The addition of adrenaline, noradrenaline or phenylephrine, but not isoprenaline to monocyte cultures enhanced synthesis of the second complement component (C2). This effect was abrogated by the concomitant addition of the receptor antagonist, phentolamine, but not the beta receptor antagonist propranolol. Thus the receptor involved is an alpha adrenergic receptor. Further studies showed that the receptor was of the alpha 1 subclass as prazosin inhibited the action of adrenergic agonists. Pulse label studies using 3H-amino acids showed that the enhancement of synthesis of eight complement components (C2, C3, C4, C5, factor B, properdin, beta 1H and C3b inactivator) and total protein synthesis were also increased. The possible mechanisms underlying these changes are discussed.

Adrenergic alpha-Agonists↗
PubMed1980

[Interferons and their importance for prevention and therapy in man and animals].

In form of a survey of the actual international literature, taking into consideration own investigations, the present stage of knowledge concerning properties of interferones, inductors, course of synthesis and therapeutic mechanism is described. The effect of the interferones is in a manifold way connected with the effect of other factors of the infection defence, with complement, properdin, activity of phagocytosis and formation of antibodies. Though the application of interferone is still connected with great difficulties, encouraging results were yielded already in respiratory diseases and in tumour diseases, too. These results justify the performance of further experiments.

Animal Diseases↗
PubMed1982

Vitamins and immunity: II. Influence of L-carnitine on the immune system.

Vitamin A affects the antibody responses and may affect phagocytic function and properdin levels. Pyridoxine deficiency impairs nucleic acid synthesis and depresses antibody formation, delayed hypersensitivity reactions and the ability of phagocytes to kill bacteria. Pantothenic acid deficiency impairs antibody formation. Vitamin C deficiency increases the incidence of infection, primary by a negative influence on reparative processes. Deficiencies of other vitamins either have not been sufficiently studied or have a variable effect. Moreover, even substances which for their biosynthesis require an adequate vitamin supplementation may exert immunomodulatory influences. With this respect the authors report their results on the influence of L-carnitine on the immune system. L-carnitine increases the proliferative responses of both murine and human lymphocyte following mitogenic stimulation and increase polymorphonuclear chemotaxis. Furthermore, L-carnitine, even at minimal concentrations, neutralizes the lipid induced immunosuppression.

Animals↗
PubMed1982

Regulation of the C3 nephritic factor stabilized C3/C5 convertase of complement by purified human erythrocyte C3b receptor.

Activation of complement may result in the generation of the amplification convertase C3bBb. This convertase can be stabilized by properdin (P) or C3NeF. C3bBbP is susceptible to inactivation by beta 1H, while C3bBbNeF is relatively resistant. Since it has been shown that the human erythrocyte C3b receptor (CR1) is able to inactivate C3bBbP, the inactivating action of CR1 on C3bBbNeF was investigated CR1 is at least five times more efficient than beta 1H in inactivating C3bBbNeF. Kinetic studies revealed that CR1 induces an enhanced biphasic kinetics of decay of C3bBbNeF; further purification of this C3NeF preparation by cation exchange chromatography showed that this phenomenon is dependent on the population of C3NeF. Finally CR1 is also able to inactivate fluid phase C3bBbNeF.

Complement Activating Enzymes↗
PubMed1983

Measles and acute glomerulonephritis.

A 5-year-old boy had transient glomerulonephritis following measles infection. Serologic studies at the early onset of the disease showed decrease of serum C3, C4, and Clq levels with normal serum properdin factor B. Renal glomerular histology revealed a mild acute proliferative glomerulonephritis. Measles virus antigen, C3, C4, and immunoglobulin G (IgG) were demonstrated in the glomerulus, suggesting an immune complex deposition. Ultrastructurally, subepithelial, intramembranous, and subendothelial electron-dense deposits were noted, suggesting a postinfectious immune complex glomerulonephritis. It is suggested that the measles virus antibody complexes are deposited in the glomerulus and activate the classic pathway of complement, leading to a self-limited glomerulonephritis.

Antigen-Antibody Complex↗
PubMed1983

Surface-dependent modulation by H of C5 cleavage by the cell-bound alternative pathway C5 convertase of human complement.

Regulation by H of formation of the C3 and C5 alternative pathway convertases of complement on cells is dependent on such chemical characteristics of the cell surfaces as their membrane content in sialic acid. Properdin-stabilized C5 convertase sites were assembled on the non-activating cells of the alternative pathway, sheep erythrocytes (Es), and on the activating cells, desialated Es and rabbit erythrocytes (Er). C5 hemolytic sites were revealed by incubation of the convertase-bearing cells with limiting C5 and excess C6-C9. H inhibited generation of C5 hemolytic sites in a dose-related fashion on Es, Er, and desialated Es at molar ratios of H/C5 of 0.03 to 0.5. H similarly inhibited C5 utilization by the cell-bound C5 convertase on Es and desialated Es regardless of the cell membrane sialic acid content; however, H was three to five times less effective on Er. Kinetic experiments also suggested that C5 hemolytic sites are generated more rapidly on Er than on Es and desialated Es. The inhibition effect of H was independent of the number of C5 convertase sites per cell on all cell types; two to three times more residual hemolytic sites were found on convertase-bearing Es that had been incubated with C5 and H as compared with cells that had been decayed by H before incubation with C5. Furthermore, H also inhibited C5 interaction with a preformed classical pathway C5 convertase. These results suggest that H interacts with C5 so as to alter C5 binding and/or cleavage by the cell-bound C5 alternative pathway convertase. Sialic acid-independent modulation by H of C5 cleavage by the C5 convertase represents an additional regulatory step in the activation of the human alternative complement pathway.

Animals↗
PubMed1984

Autoimmune phenomena in infertile patients with endometriosis.

To assess the presence of autoimmune factors in patients with endometriosis, endometrial homogenates, peritoneal fluid, and serum were evaluated in 23 patients with endometriosis and 22 control subjects. The methods used were Ouchterlony immunodiffusion, immunoelectrophoresis, polyacrylamide gel electrophoresis, and radial immunodiffusion. The study demonstrated precipitation lines between endometrial homogenates and serum from some endometriosis patients but not from the control subjects. Immunoelectrophoresis demonstrated precipitation lines at beta-globulin position when endometrial homogenates were used against serum of patients with endometriosis and with goat antihuman serum. It is suggested that an antigen, possibly a glycoprotein, is present in the endometrial homogenates. Radial immunodiffusion studies for immunoglobulins (Ig) G, A, and M and complement components C3c and C4 showed significantly higher concentrations of C3c and C4 in serum and peritoneal fluid of patients with endometriosis than the control subjects (P less than .05). There was no significant difference in concentration of IgG, A, M, factor B, and properdin.

Adolescent↗
PubMed1984

Complement deficiency states and infection: epidemiology, pathogenesis and consequences of neisserial and other infections in an immune deficiency.

Inherited deficiencies of the complement proteins are rare in unselected populations. Examination of patients with the clinical correlates of complement deficiency (autoimmune disease and certain bacterial infections) shows the frequency of inherited complement deficiency to rise enormously (5.9% of patients with systemic lupus erythematosus, 10 to 25% of adults with sporadic meningococcal disease). Autoimmune diseases of all types, but especially systemic lupus erythematosus, discoid lupus and glomerulonephritis, are seen in all categories of complement deficiency, most typically in those of the early classical pathway (C1, C4, C2). Pneumococcal infections are characteristic of deficiencies of the early classical pathway, as well. Deficiencies of C3 are associated with severe disease including autoimmune phenomena, pneumococcal and neisserial infections. C3-deficient patients become ill substantially earlier in life. Infections with N. meningitidis and N. gonorrhoeae are most typical of the late component deficiencies, with over 40% of homozygotes affected. Despite the presence of this deficiency from birth and the peak age-specific incidence of meningococcal disease in the general population at ages 3-8 months, the median age of first infection in the late component-deficient patients is 17 years. Relapse of infection is ten times more common in these patients, and discrete recurrences are seen in 45% of affected individuals. An unusual and unexplained predilection for infection with serogroup Y N. meningitidis exists. Despite an immune deficiency, and problems with ascertainment bias, it appears that persons with late component complement deficiency enjoy less mortality than normals who contract meningococcal disease. Attempts to explain the pathogenesis of neisserial infection in late component deficiencies have focused on the concept that normally non-pathogenic serum-sensitive bacteria are etiologic in the absence of serum bactericidal activity. Data to support this concept remain to be developed and contrary data exist. A separate mechanism may predispose properdin-deficient patients to meningococcal infection, since they appear to develop fulminant infections with high mortality.

Adolescent↗
PubMed1984

Activity and characteristics of inflammatory effector cells in newborns.

To investigate the aspecific activity of inflammatory effector cells (mononuclear and polymorphonuclear leukocytes) of newborn babies, a comparative study was performed of chemotactic and random filter motility, phagocytic activity, and bactericidal capacity of these cells, of the electron microscopic counterparts of these activities, the serum factors influencing motility and of the content and ratio of cyclic nucleotides present in the cells of subjects of different ages. It was found that chemotaxis of the mononuclear and polymorphonuclear leukocytes is a gradually maturing function; its deficiency observed during the neonatal period is not caused by a depressed excitability by chemical agents, by the presence of inactivators of chemotactic factors or of chemotaxis inhibitors. It is the low serum levels of total complement, C 3, IgG, IgM and properdin that explain the reduced chemotactic mobility. In addition to these factors reduced leukocyte flexibility, condition and activity of the flexibility, condition and activity of the microtubular and microfilamentary system depending on calcium ion and cyclic nucleotide concentrations, and an eventual immaturity or exhaustion of certain intracellular enzymes also play a part. In respect to orientation towards chemical stimuli, the leukocytes of the newborn largely differ from those of children or adults. Similarly, a difference in uptake and elimination of bacteria and in ultrastructural changes accompanying these processes can be demonstrated between newborn and adult cells. The aspecific cellular functions, the reduction of which plays an important part in the weak resistance of the newborn, also depend on certain properties of the infective agents.

Adult↗