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At least 1,135 records · Page 63Linked to original sources
PubMed1984

Residual hemolytic and proteolytic activity expressed by Bb after decay-dissociation of C3b,Bb.

Bb (Mr = 63,000) is the catalytic site-bearing subunit of the C3 convertase of the alternative complement pathway, C3b,Bb, which is dissociated from the complex upon decay of the enzyme. Because purified Bb induced certain leukocyte activities, we examined whether it expresses residual hemolytic or proteolytic activity. Hemolytic activity of Bb was tested by using Factor B- or Factor D-depleted normal human serum and rabbit or sheep erythrocytes. Proteolytic activity of Bb was assessed by using purified C3 or C5 as substrates and SDS-PAGE to detect protein cleavage. Bb expressed metal-dependent hemolytic activity that was approximately 100-fold lower than that of Factor B. This activity could be inhibited by Factor H and enhanced by properdin. Low but statistically significant binding of 125I-labeled Bb to C3b on erythrocytes was demonstrated. Monoclonal antibodies that bind to Bb but not to intact Factor B inhibited the Bb hemolytic activity. Purified Bb cleaved C3 to C3a and C3b, as evidenced by the appearance of the alpha'-chain of C3b. It also cleaved C5 to C5a and C5b when cobra venom factor was present in the reaction mixture. Metal ions were required for expression of proteolytic activity, and Ni supported the activity better than Mg. These results indicate that decayed Bb has residual C3 and C5 cleaving activity and hemolytic activity, expression of which appears to require its association with C3b, C3(H2O), or cobra venom factor. These observations may aid in explaining the mechanism of action of Bb on leukocytes.

Antibodies, Monoclonal↗
PubMed1983

[Evaluation of the efficiency of the immune system after immunostimulation in patients with breast cancer].

67 patients with mammary carcinoma were submitted to an immunological control examination. This control comprised 14 tests which determined the efficacy of the immune systems, among others: activity of complement, properdin, lysozyme, and beta-lysin, the rate of immunoglobulins, and the behavior of leucergy, rosette tests, NBT, BLT, and tuberculin test. The thoroughly executed examinations did not show any significant difference between patients with active neoplasms and patients in remission stage. The analysis of the results achieved for patients in an advanced stage (TNM) only showed a significant increase (p less than 0.05) of IgG in stage III/IV. The patients were treated with CVF, levamisole (Decaris), and BCG. The observation period was twelve months. The results achieved were discussed in detail.

Adult↗
PubMedDate not supplied

[Immunologic changes in the acute period of slight craniocerebral trauma].

The authors discuss the results of a dynamic study of the characteristics of nonspecific immune responsiveness (properdin, total protein and globulin fractions in blood plasma, C-reactive protein, and immunoglobulins G, A, and M) as well as of the index of water metabolism of the brain matter--the antidiuretic hormone (ADH) in plasma, in 259 patients with the nosological forms of a mild craniocerebral injury 145 of whom had concussion of the brain and 105 had mild contusion of the brain. Congruence of the clinical manifestations of the injury and the level of plasma ADH was recorded. The participation of the factors of nonspecific immune responsiveness in the body compensatory posttraumatic reactions and the genesis of the clinical manifestations of a mild craniocerebral injury is emphasized.

Acute Disease↗
PubMed1978

Blood coagulation changes in shock.

A secondary coagulopathy develops in a state of hypovolemic shock; in endotoxin shock, the coagulopathy is primary. As the changes in the hemodynamic and metabolic functions advance in hypovolemic shock, a state of hypercoagulability appears which reinforces the irreversible nature of this condition. In endotoxin shock, a primary mixed coagulopathy develops as an event directly related to the presence of bacterial lipopolysaccharides. The first finding is the activation of the fibrinolytic system through the activation of the serum complement system by means of the participation of the properdin, the so-called alternate pathway to the complement system. At the same time and by an identical mechanism, the activation of Factors VII and XI occurs through the activation of the Fletchner Factor, while the Hageman trait is activated by kinogen. Immediately after and following an antigen-antibody type reaction, endotoxin stimulates activation of platelets in the presence of gamma-2-globulin along the classical pathway of activation of the serum complement.

Animals↗
PubMed1980

The effect of Listeria monocytogenes lipids on the activity of nonspecific immune mechanisms.

The administration of Listeria monocytogenes lipids (LML) in mice resulted in the development of population of macrophages with increased phagocytic and microbicidal activity, as well as higher content of the lysosomal acid hydrolases. The elevation of the serum level of lysozyme, complement and properdin in guinea pigs after LML injection was observed. The normal macrophages cultured in vitro were also activated by LML independently on the presence or absence of autologous lymphocyte. It is concluded that the mechanism of the increase of the host resistance evoked by LML depends on the direct stimulatory effect of LML on the activity of the mononuclear phagocyte system.

Animals↗
PubMed1983

[Effect of ultrasound on cellular and humoral immunity factors].

Experiments on CBA mice were performed to explore the changes in the body immunoreactivity induced by low intensity ultrasound. A study was made of the content of lysozyme, properdine, T and B rosette-forming lymphocytes, and complement in the peripheral blood, the histophysiological properties of the lymphoid organs, and the titer of pertussis antibodies. It has been disclosed that ultrasound has a stimulant effect, primarily on the T system immunity, which was confirmed during immunization with B. pertussis vaccine. The stimulant effect has been also supported by histostructural analysis of the lymphoid organs.

Animals↗
PubMed1981

The alternate complement pathway. A possible role in a patient with focal glomerular sclerosis.

A boy had focal segmental glomerular sclerosis after the resolution of an unusual transient functional defect in activation of the alternate complement pathway. Prior to 1 year of age, the patient suffered repeated serious bacterial infections that were associated with an inability to opsonize Escherichia coli ON 2 in vitro. Serum levels of complement components were normal. Shortly after resolution of the complement defect, nephrotic syndrome developed. Properdin and C3 were identified in sclerotic glomeruli, which suggests that the ability to activate the alternate complement pathway played a role in the pathogenesis of glomerular sclerosis.

Biopsy↗
PubMed1980

Increased biosynthesis of complement components by cultured monocytes, synovial fluid macrophages and skynovial membrane cells from patients with rheumatoid arthritis.

Monocytes, synovial fluid (SF) and synovial membrane (SM) macrophages from patients with rheumatoid arthritis (RA) were maintained in short-term tissue culture for up to 10 days, and the synthesis of C4, C2, C3, C5, factor B(B), D, properdin (P), C3b inactivator (C3bINA) and beta 1H globulin studied. Functionally active C2, B, D, P, C3bINA and beta 1H were synthesized by the cells in each type of culture. C4, C3 and C5 could be detected, but were functionally inactive. RA monocytes synthesized more C2 than monocytes from patients with degenerative joint disease (DJD) (P < 0.001). Similar studies revealed that SF macrophages synthesized more C3 than SM macrophages (P < 0.001) which in turn produced more C2 than monocytes (P < 0.001). Other experiments showed that SF macrophages synthesized more of each component than the other cell types. SM macrophages made more C2 than B than RA and DJD monocytes, but synthesized only small quantities of P, D and beta 1H. RA monocytes synthesized more of each component than DJD monocytes. The results of these studies show that (1) in RA, complement components can be synthesized locally in the inflamed joints, and (2) local factors in the joints probably stimulate complement synthesis.

Arthritis, Rheumatoid↗
PubMed1982

Complement-mediated inhibition of immune precipitation. II. Analysis by sucrose density gradient ultracentrifugation.

The factors influencing the ultracentrifugation characteristics of immune complexes generated in the presence of fresh normal human serum have been analysed. In the absence of alternative pathway factors B, D or Properdin, the size of complexes was increased. When classical pathway function was blocked, in C1q deficient serum or in the presence of Mg EGTA, although the proportion of complexes remaining in solution were reduced their size was similar to those formed in normal human serum. In C2 deficient serum, a heterogeneous population of complexes was generated. In all instances repletion with the appropriate missing complement component reversed the abnormality. We conclude that there is normally a rapid sequential process of classical followed by alternative pathway activation leading to stable soluble complexes. In the absence of C1 activation the alternative pathway process requires precipitation of the antigen-antibody aggregates whereas in normal serum these events occur in the fluid phase. We suggest that in C2 deficient serum the C1 and/or C4 reacted complexes fail to activate the alternative pathway efficiently.

Animals↗
PubMed1978

Experimental bovine trypanosomiasis. Changes in serum immunoglobulins, complement and complement components in infected animals.

In three calves experimentally infected with Trypanosoma congolense the amounts of IgG1 and IgG2 were little changed and similar to those of normal animals. IgM increased in amount early in the infection and the amount of the increase appeared related to the parasite burden. The amounts of IgA and IgE were both much decreased and this also appeared related to the numbers of parasites in the blood. There was a decrease in the amounts of total haemolytic complement and complement components C1, C1q and C3 in the infected calves. Furthermore the amounts of properdin fluctuated with the cyclical changes in numbers of T. congolense parasites in the individual calves. No significant change in the amount of C8 was observed. It is considered that activation of both the alternative and the classical complement pathways occurs in trypanosome infected animals but that neither pathway goes to its terminal stages.

Animals↗
PubMed1981

Preservation of splenic function by autotransplantation of traumatized spleen in man.

Splenectomy is known to increase the risk of overwhelming bacterial infection. Characteristically, there is a decrease in immunoglobulin IgM, properdin, and T-lymphocytes; impaired primary antibody response to antigen challenge; an altered opsonic function; and a tuftsin deficiency. Because the spleen is important in host defense, preservation of traumatized splenic tissue has been advocated. Splenic autotransplantation has been suggested as a method of preserving function, and this concept is supported by experiments in animals. The present study describes autotransplantation of the traumatized spleen in human beings for the preservation of splenic function. Four patients operated on for blunt abdominal trauma required total splenectomy for hemostasis and were deemed suitable candidates for autotransplantation of the splenic tissue. In each, thinly sliced segments of spleen (roughly 20 gm.) were placed in a previously fashioned omental pouch. All patients survived without complications. Postoperative studies included blood and platelet counts, cell morphology, determination of serum immunoglobulin levels, and splenic scans. Four weeks postoperatively, Howell-Jolly bodies and target cells had disappeared from the red cells. Platelet counts returned to normal range. Initially low IgM and C3 complement levels increased to normal. Scans at 8 weeks confirmed the presence of functioning splenic tissue. Autotransplantation of the spleen is a safe method for preserving splenic function when total splenectomy is mandatory for hemostasis.

Adolescent↗
PubMed1994

Nephrotic syndrome associated with subacute bacterial endocarditis (SBE): a case report.

We experienced a female nephrotic patient associated with subacute bacterial endocarditis. Her proteinuria was completely normalized after antibiotic therapy and valve replacement. Immunofluorescence and an electron microscopic study of a renal biopsy specimen showed little evidence of immune complex in the glomeruli. Marked deposition of properdin in the glomeruli and the reduced level of serum complement may indicate involvement of the complement system in the pathogenic mechanism of massive proteinuria in this case.

Adult↗
PubMed1977

Hageman complement and factor.

Complement components are activated by immunologic and non-immunologic mechanisms through various plasma protein systems such as immunoglobulins, properdin, plasmin, thrombin and Hageman factor. The activation of Hageman factor, followed by complement cleavage leading to liberation of various chemical mediators, can be initiated by exposure of negatively charged tissue components due to trauma and infection.

Blood Coagulation↗
PubMed1977

Breakdown products of C3 and factor B in hemolytic-uremic syndrome.

Serum concentrations of Clq, C4, C3, and Factor B but not properdin were significantly decreased in patients with HUS compared to values in normal control subjects (p value less than 0.01). Sera from 13 HUS patients obtained early after the onset of the disease showed breakdown products of Factor B (Ba, Bb) by immunoelectrophoresis; 12 of these sera showed C3 breakdown products (C3c, C3d). Sera from seven patients studied 1 month to 3 years later no longer demonstrated any breakdown products of Factor B or C3. These data suggest that the complemented system is activate in HUS. The concept that immunological mechanisms play a major role in this disease is additionally supported by the occurrence of IgM, C3, and fibrin in glomeruli and renal vessels.

Adolescent↗
PubMed1996

Identification of complement activation sites in human immunodeficiency virus type-1 glycoprotein gp120.

Recombinant glycoprotein 120 (rgp120) of human immunodeficiency virus type-1 (HIV-1) activates the human complement system in the absence of anti-gp120 antibodies. HIV-1 glycoprotein gp120 can dissociate from the viral envelope either spontaneously or after binding of HIV-1 to the CD4 molecule. As a consequence, gp120 can circulate in the patient's serum and attach to the surface of uninfected CD4+ T cells. Complement activation by cell-bound HIV-1 glycoprotein gp120 with subsequent opsonization may represent a mechanism for the elimination of uninfected CD4+ cells by the reticuloendothelial system, thereby enhancing the progression of HIV disease. In the current study, the complement proteins C4,C3,C5,C9, and properdin were found to bind to a synthetic peptide covering positions 233-251 of the gp120BRU sequence on incubation with normal human serum. Complement activation by the peptide was comparable with that induced by aggregated IgG, complete rgp120, and the previously described complement-activating gp41-peptide 609-623. Activation occurred via the classical pathway and was abrogated in the presence of EDTA, Mg2+/EGTA, or C4-deficient human serum. Peptides partly overlapping the sequence 233-251 activated complement to a lesser extent. The complement-activating capacity of the gp120 sequence 233-251 was not restricted to the HIV-1BRU isolate, because a peptide from the corresponding sequence of the HIV-1MN strain was also capable of activating complement. An additional strong complement-activating site was identified in the gp120 sequence 321-360 of the HIV-1MN strain. These data indicate that distinct sites in gp120 are able to activate human serum complement via the classical pathway in the absence of anti-gp120 and independent of glycosylation.

Amino Acid Sequence↗
PubMed1977

[Complex laboratory-morphologic study of allergic joint inflammation in rabbits].

During the period of sensitization and in the dynamics of the development of the articular allergic inflammation in rabbits there occured regular slowing down of the properdin activity, decrease in the compliment titres and increase in the blood plasma magnesium content. An increased liability of the basophilic leukocytes to damage and an elevated activity of acid phosphotase in lymphocytes of the peripheral blood were also noted. In the acute period of inflammation the synovial sheaths were found to be diffusibly infiltrated by the lymphoid-histocytic and plasma cells. Proliferation of synoviocytes and the appearance therein of the PAS-positive granules were observed. Weakening of the myocardial staining with Schiff's reagent was established. The processes of disorganization of the connective tissue in a joint and in the heart were closely conjugated and manifested themselves in mucoid and fibrinoid swelling, and changes in the PAS-reaction. Dissociation of the natural resistance of the organism was revealed: mobilization of the processes of immunogenesis and inhibition of the nonspecific link of protection. Decrease in the immunological reactivity was associated with formation of hypersensitivity of delayed type. Cosequently, arthritis developed in rabbits on the immune basis.

Animals↗
PubMed1977

Mechanism of complement activation by radiographic contrast media.

Activation of the complement system by radiographic contrast media (RCM) was demonstrated by in vitro haemolytic and immunological assays. Such activation was found to be a function of the RCM molar concentration. Iodipamide was the most active of five RCM tested. When RCM was incubated with normal human serum (NHS) in the presence of ethylene glycol-tetra-acetic acid and magnesium ions, conditions which block activation of the classical pathway but permit activation of the alternative pathway, haemolytically active C3, properdin and factor B were found to be decreased but haemolytically active C4 was normal. Using counterimmunoelectrophoresis, the activation of complement was further demonstrated by detection of C3 and factor B-split products. Finally, when radiolabelled complement proteins were reacted with RCM in vitro and studied by density-gradient ultracentrifugation, it was demonstrated that a large complex was formed with a sedimentation of 22S, similar in characteristics to the C5b-C9 complex. It was postulated that the mechanisms of in vitro consumption of complement by RCM was mainly through the alternative pathway.

Complement C3↗
PubMed1976

The complement profile in babesiosis.

Rats have been infected with Babesia rodhaini, a protozoan agent that induces immune complex disease. Assays for complement have revealed depletion of C2, C3, C4, C5, and whole complement in the course of infection. No evidence of depletion in the alternative (properdin) pathway was found. These findings are consistent with the conclusion that the classical complement pathway is activated during the course of the protozoan infection.

Animals↗