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PubMed1980

Covalent binding and hemolytic activity of complement proteins.

We report the inactivation of the third component of complement (C3) by hydroxylamine. C3 hemolytic and covalent binding activities decline with identical kinetics, demonstrating a direct correlation between the two activities. We conclude that covalent, surface-bound C3b is hemolytically active. The inactivation of C3 is first order with respect to hydroxylamine. We also studied C3 inactivation with [14C]methylamine. The inactivation corresponds quantitatively with the labeling of C3 in the C3d domain. The data obtained support the following hypothesis: there is an internal thioester within C3 which becomes highly reactive on activation to C3b, and C3b binds to receptive surfaces by transfer of the acyl function of the thioester to a hydroxyl group on the receptive surface. This proposed model for the reaction of C3 with receptive surfaces also applies to C4, which binds to membrane surfaces covalently and is able to be inactivated by hydroxylamine and methylamine. C5, on the other hand, is not inactivated by treatment with the amines.

Binding Sites↗

PubMedDate not supplied

Effect of complement and polymorphonuclear leukocyte depletion on experimental skin lesions resembling systemic lupus erythematosus.

Immunopathologic cutaneous lesions resembling human systemic lupus erythematosus (SLE) can be induced in mice sensitized to ultraviolet (UV)-irradiated DNA following whole body irradiation with UV light. The lesions are characterized by the formation of immune complexes at different skin sites. The role played by cellular and humoral mediators in the pathogenesis of this experimental model was investigated. The results obtained suggest that inflammation that follows UV radiation is the major factor responsible for this pathology. Accordingly mice that were rendered neutrophil PMN) deficient did not manifest skin lesions, and depletion of C3 complement component left them unchanged. In addition time course studies showed that PMN depletion did not prevent a delayed skin involvement. Thus multiple factors seem to mediate the onset of the immunopathologic changes previously described.

Animals↗

PubMed1985

Biocompatibility of cuprophan and cellulose acetate membranes. Prevention of dialysis hypoxemia and leucopenia by ticlopidine.

The study is a comparison of 4 successive hemodialysis (HD) sessions on each patient, 2 with cuprophan (CU) membrane (Gambro 120 M) and 2 with Cellulose acetate (CA) (Cordis Dow 3500). 60 minutes prior to the HD session placebo or Ticlopidine (500 mg) was administered orally to each patient. Leucocyte and platelet counts, serum C3 complement, arterial PO2, PCO2 and PH were measured before and 15, 30, 60, 120 and 240 minutes after the beginning of HD. Leucocyte count fell markedly within 15 minutes of both placebo HD sessions, but it was significantly lower (p less than 0.005) in CA than CU membrane. Ticlopidine prevented significantly (p less than 0.01) the HD-induced leucopenia. Slight changes in platelet count, either in placebo or Ticlopidine study were observed. Serum C3 complement increased significantly (p less than 0.05) at 15 minutes of CU placebo session and was also correlated (p less than 0.01) with the concurrent leucopenia. The arterial PO2 decreased 22% and 13.5% during HD with CU and CA membranes respectively, but it was preserved within normal limits by Ticlopidine. The arterial PH was increased up to 7.4 at the end of all HD sessions, while PCO2 showed only slight changes. We conclude that: 1) CA membrane is better tolerated than CU 2) HD-induced leucopenia and hypoxemia are prevented by Ticlopidine, probably by modulating the complement activation.

Adult↗

PubMedDate not supplied

Autoantibodies, immunoglobulins, complement and circulating immune complexes in acute malaria.

BACKGROUND: Malaria caused by Plasmodium vivax and Plasmodium falciparum is common in the Indian subcontinent. Studies conducted elsewhere have suggested that malarial infection causes intense immunostimulation. We screened patients with malarial infection for autoantibodies and measured the immunoglobulin, circulating immune complex and complement levels to determine the extent of immunological alterations in these patients. METHODS: One hundred adults with acute malarial infection confirmed by examination of the peripheral blood smear and 25 age- and sex-matched controls were studied. An autoantibody screen and serum immunoglobulin complement (C3 and C4) and circulating immune complex levels were measured at the time of admission and 4 weeks after they became afebrile. A direct Coomb's test was also done. RESULTS: Anti-ssDNA, anti-dsDNA and rheumatoid factor were positive at the time of admission in 51, 30 and 38 patients respectively. None of the controls were positive for these autoantibodies except for one who was positive for rheumatoid factor. The IgM, IgG and IgA levels were raised in 16, 25 and 36 patients respectively. Circulating immune complex levels were raised in 32 patients and complement C3 and C4 were low in 8 and 31 patients. Follow up studies at 4 weeks in 19 patients showed that the autoantibodies were negative. However, the immunoglobulin, C4 and circulating immune complex levels remained elevated. Six per cent of patients had a positive direct Coomb's test with reticulocytosis at the time of presentation. CONCLUSION: Acute malarial infection can cause false-positive results for anti-ssDNA, anti-dsDNA and rheumatoid factor and may also cause a rise in the serum immunoglobulin, complement and circulating immune complex levels.

Adolescent↗

PubMed1992

Calcium depletion blocks proteolytic cleavages of plasma protein precursors which occur at the Golgi and/or trans-Golgi network. Possible involvement of Ca(2+)-dependent Golgi endoproteases.

The effects of calcium depletion on the proteolytic cleavage and secretion of plasma protein precursors were investigated in primary cultured rat hepatocytes and HepG2 cells. When the cells were incubated with A23187, the calcium-specific ionophore, in a medium lacking CaCl2, precursors of serum albumin and the third and fourth components of complement, C3 and C4, respectively, were found to be released into the medium. The addition of ionomycin or EGTA to the medium inhibited the processing of pro-C3 as well. Blocking the secretory pathway either at the mixed endoplasmic reticulum/Golgi in the presence of brefeldin A or at the endoplasmic reticulum/tubular-vesicular structure at a reduced temperature caused accumulation of pro-C3 within hepatocytes or HepG2 cells, indicating that the cleavage of the precursor occurs at a later stage of the secretory pathway. Once the blockade was released by incubating the cells either in the brefeldin A-free medium or at 37 degrees C, the secretion of plasma proteins resumed, irrespective of the presence of A23187. However, the processing of pro-C3 was almost completely inhibited in the presence of A23187, with only the precursor being released into the medium, implying that a decline in Ca2+ levels within the cell modulates the activity of a Golgi endoprotease responsible for the cleavage of pro-C3. When incubated with isolated Golgi membranes, pro-C3 secreted from Ca(2+)-depleted cells was cleaved in vitro into their subunits in the presence of Ca2+ but not in its absence, pointing to the involvement of a Ca(2+)-dependent Golgi endoprotease in the processing of pro-C3. These results collectively suggest that calcium depletion blocks the proteolytic cleavages of plasma protein precursors presumably by exhausting a Ca2+ pool available to the Ca(2+)-dependent processing enzyme(s) located at the Golgi and/or trans-Golgi network.

Animals↗

PubMed1972

Role of antibody and complement in the immune clearance and destruction of erythrocytes. II. Molecular nature of IgG and IgM complement-fixing sites and effects of their interaction with serum.

A model for the immune clearance and destruction of homologous erythrocytes has been further explored. In this model, every IgM anti-erythrocyte antibody molecule in an antibody preparation was shown to fix Cl. About 2000 IgG antibody molecules were required to form a Cl-fixing site on the guinea pig erythrocyte surface. 60 IgM complement-fixing sites per erythrocyte were required for the immune clearance of IgM-sensitized erythrocytes. This number of sites could be detected by a direct agglutination test. 1.4 complement-fixing sites were required for immune clearance of IgG-sensitized cells, a number of molecules which could not be detected by direct agglutination. This number could, however, be detected with the use of a Coombs antiglobulin reagent. Depletion of the late components of complement (C3-9) with cobra venom was associated with the loss of ability to clear IgM-sensitized cells and a marked deficit in the ability to clear IgG-coated cells. Thus, late (C3-9) components of complement as well as an early component (C4) were required for normal clearance of sensitized erythrocytes. There was no evidence that activation of the alternate pathway of complement action could lead to accelerated erythrocyte clearance. In vitro incubation of IgG and IgM-sensitized erythrocytes in fresh serum led to deposition of C3 and C4 on the erythrocyte surface. IgM-sensitized cells treated in this way had a normal survival. IgM-sensitized cells also were shown to remain Coombs positive after their release from the liver. The evidence suggests that the interaction of an IgM site with fresh serum in vitro and in vivo leads to formation of a site which allows for sequestration of cells in the liver. With continued exposure to serum components, this site is destroyed or inactivated. This serum-dependent inactivation is complement-dependent as shown by the use of EDTA-treated and C4-deficient serum. IgG complement-fixing sites are only partially inactivated by incubation in fresh serum, further emphasizing the differences in the biologic activity of IgM and IgG antibodies.

Animals↗

PubMed2005

Role of complement and B lymphocytes in Sjögren's syndrome-like autoimmune exocrinopathy of NOD.B10-H2b mice.

Sjögren's syndrome (SjS) is a human autoimmune disease characterized by the loss of exocrine function as a result of a chronic immune attack directed primarily against the salivary and lacrimal glands leading to xerostomia (dry mouth) and xerophthalmia (dry eyes). NOD.B10-H2b mice manifest many features of SjS, exhibiting exocrine gland dysfunction concomitant with leukocyte infiltration of the salivary and lacrimal glands. Recent studies have shown that both SjS patients and NOD.B10-H2b mice exhibit increased B lymphocyte survival, B cell hyper-reactivity and hyper-gammaglobulinemia with high production of autoantibodies. To study the possible influence of complement on the development and expression of SjS-like disease of the NOD.B10-H2b, we have utilized a prophylactic treatment with CVF known to interfere with the action of complement C3 factor. NOD.B10-H2b mice, injected with CVF starting at 10 weeks of age, a time when leukocyte infiltration is expected to begin, failed to develop salivary dysfunction out to 24 weeks of age, a time when reduced salivary flow rates are known to occur in non-treated animals. Concomitant with retention of salivary exocrine function, CVF-treated mice showed reduced levels of leukocytic infiltration, reduction of anti-nuclear autoantibodies and major alterations in the B lymphocyte profiles while maintaining general pathophysiological measures of disease. These data suggest that C3 plays a significant role in development and onset of SjS-like disease, yet additional studies need to be carried out to identify the precise mode of action.

Animals↗

PubMed1991

[Immunopathological study of synovium of rheumatoid arthritis].

46 patients with different rheumatic disorders were subjected to arthroscopic examination and the biopsied synovia were studied immunopathologically. Immunoglobulins, complements and fibrinogen deposition were detected by direct immunofluorescence, and rheumatoid factor (RF) deposition was detected by peroxidase-labelled denatured human IgG. Postoperative diagnosis of these cases were as follows: rheumatoid arthritis (RA) 21; seronegative spondylarthropathy 4; reactive arthritis 2; unidentified synovitis 4; osteoarthritis 8; and nonsynovitis conditions 5. It was shown that the positive rates of deposition of IgG, IgM, complement C3, C1q and C4, and RF in RA were 95.2%, 52.4%, 38.1%, 28.6%, 9.5% and 42.9%, respectively. Deposition was negative in all other rheumatic diseases. The positive fibrinogen deposition rate in RA was 42.9%; it was weakly positive in other disorders as well. The results indicate that the pathogenesis of RA is related to humoral immunity, and immunopathological study of the synovium has very important diagnostic significance in RA. On the other hand, deposition of fibrinogen lacks specificity for any rheumatic disease. The deposition of RF IgG, IgM and complement C3, C1q and C4 in the synovium of RA patients does not correlate well with clinical disease activity. The deposition of RF in the synovium also does not show paired correlation with blood IgM RF determination. This difference may be explained by the fact that the synovial RF examined in the present study may include all isotypes of RF and that hidden-RF in the blood may give a negative result. The synovium is the site of production of RF, but the degree of pathological change of the synovium of different joints in a single patient may not be uniform. The results of humoral immunity studies of the RA synovium may be influenced by the site selected for synovial biopsy.

Adolescent↗

PubMed1990

Changes in serum proteins (albumin, immunoglobulins and acute phase proteins) in pulmonary tuberculosis during therapy.

Serum levels of three immunoglobulins (IgG, IgA & IgM), albumin and six acute phase proteins (alpha 1-antitrypsin, haptoglobin, transferrin, alpha 2-macroglobulin, complements C3 & C4) were measured by immunoelectrophoresis in 57 patients with pulmonary tuberculosis when they were first diagnosed, and followed at 1 month, 2 month and 4 month intervals during anti-tuberculosis treatment. These values were compared to those from 41 healthy controls. Significant increases were observed in the initial values of serum IgG, IgM, alpha 1-antitrypsin and haptoglobin, while transferrin and alpha 2-macroglobulin levels were significantly reduced. No changes were observed in the levels of serum albumin, IgA and complement C3. Levels of all measured proteins decreased with treatment. However, at 4 months, IgG and alpha 1-antitrypsin were still significantly elevated when compared to control values, while the level of haptoglobin had decreased to a level significantly lower than that of the control value.

Acute-Phase Proteins↗

PubMed1994

The contribution of resting heart rate and routine blood tests to the clinical assessment of disease activity in systemic lupus erythematosus.

OBJECTIVE: To contrast the contribution of simple clinical tests, such as resting heart rate (HR), complete blood count (CBC), and erythrocyte sedimentation rate (ESR), versus immunological tests in the assessment of disease activity in systemic lupus erythematosus (SLE). METHODS: During an evaluation of disease activity indices in SLE, 39 patients had a full clinical evaluation in 99 visits including a disease activity index (MEX-SLEDAI), and serial measurements of HR, ESR, CBC, complement (C3, C4) and anti-dsDNA antibody levels (Farr). RESULTS: Resting HR exhibited the highest correlation with MEX-SLEDAI scores (rs = 0.62). Thus, the disease was active (MEX-SLEDAI score of 2 or more) in all but one of 15 patients (93.3%) that had an HR > 90/min during the study. Hemoglobin levels (Hb) and ESR showed the second highest correlation (rs = -0.51, and 0.50, respectively). Seventeen patients had an Hb < 13 g/dl at least once; 14 (82.4%) had active disease during the study. Lymphocyte count, C3 levels, and anti-dsDNA levels correlated less strongly with disease activity (rs = -0.27, -0.29, and 0.30 respectively). Forward stepwise multiple regression analysis showed that HR, Ht, and C3 were independent markers of disease activity in this population (R2 = 0.51, p < 0.0001). CONCLUSION: Closer attention to resting HR and CBC results may improve the assessment of disease activity in SLE.

Adolescent↗

PubMedDate not supplied

Growth control of activated, synchronized murine B cells by the C3d fragment of human complement.

Three restriction points control the cell cycle of activated B lymphocytes. The first occurs directly after mitosis and is controlled by the occupancy of surface-bound immunoglobulin. The second is observed approximately 4 h after mitosis in the G1 phase of the cycle, that is, before DNA replication, and is controlled by growth factors that are produced by macrophages which we have previously classified as alpha-type factors. The third restriction point occurs in the G2 phase, 2-4 h before mitosis, and is controlled by beta-type growth factors probably produced by helper T lymphocytes. The third component of complement, C3, has long been implicated in the control of B-cell responses. C3 is secreted by monocytes and macrophages. We have found recently that crosslinked, but not soluble, human C3 stimulates activated, but not resting, murine B cells to thymidine uptake. Here we investigate the role of C3b and C3d in the progression of the cell cycle of activated, synchronized murine B cells. We find that crosslinked C3d replaces the action of alpha-factors within the cell cycle of these cells and allows entry into S phase. In contrast, soluble C3d inhibits the action of alpha-factors. This implies that a C3d-specific receptor, probably the murine analogue to the human complement receptor CR2, is a growth factor receptor on activated B cells that will give the cell a growth-positive signal when it is crosslinked, while occupancy by the soluble form of C3d will result in inhibition of the action of alpha-factors or of crosslinked C3b or C3d. A stretch of weak homology between the cDNA sequence of murine C3d and those of murine growth factors indicates that an insulin-like growth factor could be the active principle of C3d that controls the cell cycle of activated B cells.

Animals↗

PubMed1975

Deposits of immunoglobulins and complement in the dermoepidermal junction of patients with anaphylactoid purpura.

Skin biopsies from 3 patients with anaphylactoid purpura examined by an immunofluorescence technique revealed deposits of immunoglobulins, complement C3, and fibrinogen in the dermo-epidermal junction and in vessel walls of clinically involved as well as uninvolved skin. The deposits in the dermo-epidermal junction are similar to those seen in the skin of patients with systemic lupus erythematosus.

Aged↗

PubMed1995

Changes in wound healing factors in liver cirrhosis after esophageal transection for esophageal varices.

Quantitative changes in plasma wound healing factors in cirrhotic patients after esophageal transection were evaluated and compared with those of non-cirrhotic esophageal cancer patients (controls) after esophageal resection. Serum total protein, albumin and fibronectin were maintained at the same levels as those in controls when multiple units of fresh frozen plasma and albumin products were employed. Nevertheless, the principle protease inhibitors including alpha-1-antitrypsin and alpha-1-acid-glycoprotein showed little increase by the 3rd postoperative day, while those of controls increased as much as twofold at this time. Levels of complements C3 and C4 showed consistent depression, with little change during the study period. We conclude that the levels of some of the plasma proteins essential in wound healing are depressed in cirrhotic patients during the critical period after surgery.

Blood Proteins↗

PubMed1986

[Immunological changes in the exacerbated form of chronic obstructive pulmonary disease].

Ninety four subjects were examined, 42 of them with chronic obstructive pulmonary disease (COPD) and 52--healthy. The following indices followed up: immunoglobulins G, A, M, fraction of the complement--C3 and C4, alpha 2-macroglobulin (alpha 2MG), alpha 1-antitrypsin (alpha 1 AT). The following methods were applied: radial immunodiffusion according to Manccini et al and counter-electrophoresis on cellulose-acetate. Antisera and standards of the firm "Behring"--FRG were used. The data obtained are compared with those from the group the healthy subjects. Changes were established, manifested in increased level of immunoglobulin (IgG) and considerable reduction in the values of alpha 1AT, in the patient, with exacerbated form of COPD. No substantial deviations in IgA, complement fractions and alpha 2MG were established.

Adult↗

PubMed1976

Effect of sulfones on complement deposition in dermatitis herpetiformis and on complement-mediated guinea-pig reactions.

The role of complement and the mechanism of sulfone action in dermatitis herpetiformis (DH) have not yet been established; prior studies have presented conflicting data regarding the effect of sulfones on complement activation and deposition. Thirty-eight DH patients were studied. Twenty-four of 25 perilesional skin biopsies and 50 of 67 normal-appearing skin biopsies showed the third component of complement (C3) deposited in areas corresponding to those of IgA deposition. Nine of 10 patients with bound C3 in normal-appearing and perilesional skin during periods of active disease continued to have C3 in normal-appearing skin when treatment with sulfones kept them completely free of lesions for 2 to 8 weeks. When either Hartley-strain or C4-deficient guinea pigs were given up to 150 mg/kg sulfoxone (a water-soluble sulfone) intraperitoneally for 8 days before elicitation of active Arthus, reverse passive Arthrus reactions, or Forssman shock, there was no difference in time course, character, or intensity of reactions when compared to saline-treated control animals. We were therefore unable to demonstrate any effect of sulfones on complement deposition in DH skin or on complement activation in classical or alternate complement pathway-mediated guinea-pig reactions.

Animals↗

PubMed1999

[Concentrations of selected acute phase proteins and immunity immunoglobulins in the treatment of head and neck carcinomas].

Despite the constant development of diagnostic and therapeutic methods, there is no specific test for patients with head and neck carcinoma, which can help in the early diagnosis, monitoring of the follow ups. The thesis of that paper were accompanied with remark that in many cases there is a level of change of some acute phase protein and immunity immunoglobulins. The research group consisted of 146 men and 15 women, together 161 patients with head and neck carcinoma. 114 patients with larynx carcinoma, 32 with oral carcinoma, 7 with carcinoma of ethomaxillary area, 6 with parotid gland carcinoma and 2 with ear carcinoma. Patients were divided into 5 groups. The first group (52 patients) with diagnosed carcinoma before treatment, second group (33 patients) with confirmed recidivation after treatment, third group (20 patients) after radiotherapy with no recidivation, fourth group (31 patients) after surgery treatment with no recidivation, fifth group (25 patients) after combined treatment with no recidivation. Sixth group (30 patients) was a control group. Particular acute phase proteins serum level were measured; C-reactive protein (CRP), haptoglobin (HPT), transferrin (TRF), protein C3 complement, immunity albumin's IgA, IgG, IgM. The results of five groups were compared with results of control groups. One of the ground of the statistically analyzed results were possible to draw such conclusions: 1. C-reactive protein, haptoglobin, transferrin serum levels have a significant correlation to carcinoma process. 2. Manifestation of carcinoma recidivans after treatment causes statistically significant change of C-reactive protein and haptoglobin concentration. 3. After radical antineoplasmatic treatment there is a return of C-reactive protein and haptoglobin concentration to normal level. 4. Protein C3 complement and immunity immunoglobulins medium serum levels were normal and there were no differences compare to control group.

Acute-Phase Proteins↗

PubMed1991

Humoral immune response of normal rhesus monkeys during primaquine administration.

Humoral immune response of normal rhesus monkeys was studied after giving a standard dose of primaquine. The drug did not effect the level of complement (C3) and its haemolytic activity. Levels of Immunoglobulin i.e. IgG, IgM & IgA and number of immunoglobulin secreting cells also remained unaffected. Results of this study suggested that primaquine did not suppress the immune status of the host and could be given safely to the malaria patients.

Animals↗

PubMed1981

Immunoglobulins, haemolytic complement and serum C3 in cattle infected with malignant catarrhal fever herpesvirus.

Serum levels of the third component of complement (C3) were reduced only in the terminal stages in malignant catarrhal fever (MCF) virus-infected steers. Haemolytic complement and immunoglobulin (IgM, IgG1 and IgG2) levels were not altered. C3 and immunoglobulin deposits were also not demonstrated in the vascular lesions induced by MCFV. MCF virus infection of cattle is probably not a typical immune complex-mediated disease as previously suggested.

Animals↗