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[Complement system during hemofiltration in patients with multiple organ failure].

Nine patients (8 men and 1 woman) were treated. Sepsis was diagnosed in 7 of them. All patients were subjected to forced ventilation of the lungs, 6 were in need of inotropic support. The severity of clinical status was 31 +/- 0.8 according to APACHE II score. One patient survived. The main method of substitute renal therapy (SRT) was permanent hemofiltration with spontaneous arteriovenous perfusion. The results indicate manifest depletion of the complement system augmenting with the progress of multiple organ failure (MOF). Extracorporeal perfusion in SRT had no additional negative effects on the complement system damaged by disease. Nonselective penetration of individual complement fractions into the filtrate in the course of perfusion was noted. Therefore, the complement system is severely damaged in patients with MOF; it can modulate the SRT because of penetration of its individual fractions.

APACHE↗
PubMed1978

Binding of soluble immune complexes to Raji lymphocytes. Role of receptors for complement components, C1q and C3-C3b.

We have found that, although the binding of particulate antigen-antibody complement complexes such as EAC to lymphoblastoid Raji cells is mediated largely through receptors for C3b, the binding of complement-containing soluble complexes such as those prepared with aggregated human IgG (AHG) occurs also via receptors for C1q. Evidence supporting this conclusion included: (1) Binding of AHG to Raji cells takes place after incubation in EDTA serum; (2) Binding of AHG does not occur in C1q deficient EDTA serum but does take place after addition of C1q; (3) The extent of binding of AHG in EDTA serum is a function of the amount of C1q present; (4) Raji cells can bind up to 5-4 times 10(5) molecules of 125I C1q per cell which can be blocked by unlabelled C1q; (5) AHG pre-incubated with C can bind to a T-cell line MOLT, which lacks receptors for C3b but possesses receptors for C1q to the same extent as Raji cells; (6) Immunoassays for immune complexes in human sera yield similar results whether Raji cells, MOLT cells or C1q precipitation is used for assay; (7) EAC-Raji cell rosettes can be inhibited with inulin-treated, C1q deficient serum containing C3b or C3d whereas binding of AHG or immune complexes in patient samples to Raji or MOLT cells is not inhibited by this reagent. We conclude that receptors for C1q on certain B and T lymphocytes may play an important role in physiologic functions of lymphocytes depending on binding of soluble immune complexes to their surfaces.

Antigen-Antibody Complex↗
PubMed1979

Activation of the alternative pathway of complement by antiserum to factor B.

Monospecific rabbit and goat antisera to human complement proteins and human immunoglobulins were tested for their ability to activate the alternative complement pathway. This activation was detected by two methods where classical pathway activation was blocked with EGTA and alternative pathway activation was promoted with added magnesium ions. These two methods consisted of lysis of GSHE and conversion of factor B into split products. C1q-depleted serum was used in a third assay system. Only antiserum to human factor B was able to activate the alternative pathway in the various systems used. None of the other anticomplement sera showed such activity. When antiserum to factor B was fractionated by ammonium sulfate and column chromatography, activation of the alternative pathway was found in the IgG fraction, and this activity was completely removed by absorption with purified factor B but not with other purified complement components.

Animals↗
PubMed1975

Evidence for complement activation by the alternate pathway in the arthritis of hypogammaglobulinemic patients.

The chronic, rheumatoid synovitis in four patients (two children and two adults) with immunodeficiency was studied by means of immunopathological examination of synovial tissues and fluids. Their immunodeficiencies were extensively studied, with various tests for humoral and cell-mediated immunity. The two children were boys with Bruton's disease. One adult, female, had common variable immunodeficiency. One adult male had severe hypogammaglobulinemia. All patients had isolated deposits of complement component C3 in their synovial membranes, usually without traces of immunoglobulins. Depressed levels of complement component C3 were found in the joint fluid, in contrast to high levels in the corresponding serum in one patient. Components of the alternate pathway, properdin and C3A, were found in the tissues, but not components of the classic pathway, C1q and C4. The findings suggest that chronic, rheumatoid arthritis in hypogammaglobulinemic patients may be related to activation of C3 by the alternate pathway.

Agammaglobulinemia↗
PubMed1979

Staphylococcus aureus opsonization mediated via the classical and alternative complement pathways. A kinetic study using MgEGTA chelated serum and human sera deficient in IgG and complement factors C1s and C2.

Staphylococcus aureus opsonization was studied kinetically by: (1) determination of the uptake of [3H]-thymidine labelled bacteria by human PMN's; (2) fluorescent anti-C3 and anti-IgG staining of opsonized bacteria; and (3) measuring bacterial complement consumption. Maximum opsonization in normal serum occurred within 5 min of incubation. About 80% of staphylococci were then taken up by PMN's, and IgG and C3b could be detected on the bacterial surface. In the absence of a functional classical complement pathway, as in sera deficient in C1s and C2 and in MgEGTA chelated serum, maximal opsonization was only achieved after 30--60 min incubation. Opsonization in IgG deficient serum occurred at a rate similar to that found in C2 deficient or MgEGTA chelated serum. Opsonization was greatly enhanced when sera were reconstituted. It was concluded that in IgG deficient serum Staphylococcus aureus opsonization is mediated via the alternative complement pathway. Dilution of normal serum primarily affected the classical complement pathway, resulting in a decreased rate of opsonization. In normal serum IgG did not appear to be a rate-limiting factor. S. Aureus opsonization was best studied by the phagocytosis assay and the fluorescent-antibody technique. Measuring haemolytic complement consumption was found to be an insensitive indicator of bacterial complement activation and opsonization.

Complement Activation↗
PubMed1975

The complement system in bullous pemphigoid. III. Fixation of C1q and C4 by pemphigoid antibody.

By in vitro complement immunofluorescent staining methods, 46 serum samples from bullous pemphigoid patients with titers of antibasement-membrane-zone antibodies of 320 or greater were tested for their ability to fix C1q, C4, and C3. All three staining reactions were positive with 23 of the samples; 21 samples yielded negative reactions. With one sample, the C1q and C3 staining reactions were positive but the C4 reaction was negative; one other sample gave a positive C3 staining reaction only. Absorption of anti-C1q, anti-C4, and anti-C3 with C1q, C4, and C3, respectively, blocked the specific in vitro complement staining. Therefore, bullous pemphigoid antibodies of the IgG type appear to be capable of activating the "classical" complement pathway.

Autoantibodies↗
PubMed1975

Complement deposition in glomerular diseases.

Biopsies from 400 patients affected by glomerular diseases, both "primary" and secondary to systemic diseases, have been studied by immunofluorescence. Staining was performed for immunoglobulins fibrogen and C1q, C4, C3 and C3A. C1q, C4 and C3 were positive in a high percentage of cases in focal glomerulosclerosis, membranoproliferative glomerulonephritis, lupus nephritis and essential cryoglobulinaemia glomerulonephritis. C1q and C4 were very rarely present in focal proliferative glomerulonephritis and rheumatoid purpura glomerulonephritis. C3A was found frequently only in acute glomerulonephritis. Results are discussed with reference to their diagnostic value and to information about mechanisms of complement activation.

Complement C1↗
PubMed1975

Group A streptococcal M protein vaccine: protection following immunization via the respiratory tract.

Previous studies have shown the efficacy of parenteral immunization of volunteers with purified type 1 M protein against challenge with homologous streptococcui (J. clin, Invest. 52: 1885, 1973). A double-blind study was conducted on 21 adults immunized by aerosol-spray into the nasopharynx, and 23 controls who received saline placebo. Two booster doses were given at monthly intervals and approximately 30 days later vaccinees and controls were challenged with homologous streptococci (10-6/ml) by swabbing the pharyngeal-tonsillar areas. Throat cultures, leukocyte counts, temperatures and physical signs and symptoms were followed to assess infection. Illness was defined as a positive throat culture, oral temperature of larger than or equal to 38 degrees C, a WBC count of twice baseline or greater than 10,000 per mm-3, exudative pharyngitis and adenopathy. Of the 43 subjects, 13 were ill by all criteria (10 controls, 3 vaccinees [p smaller than .02]); 21 were well by all criteria (6 controls and 15 vaccinees); and 10 exhibited some but not all positive criteria (7 controls, 3 vaccinees). Positive throat cultures following challenge were obtained in 19 controls and 5 vaccinees (p smaller than 0.001). There was no correlation between the pre-challenge serum antibody titer and the development of subsequent illness. It is concluded that local topical immunization with a M protein vaccine offers significant type-specific protection against challenge with streptococci.

Administration, Intranasal↗
PubMed1975

Receptors for immunoglobulin and complement on human alveolar macrophages.

Specific cell membrane surface receptors for immunoglobulin and complement components were identified by rosette formation on in vitro cultured alveolar macrophages obtained from 24 humans and from rabbits. Respiratory macrophages have easily identified receptors for IgG and the C3b fragment of the third component of complement. A macrophage receptor for the C3d fragment was detected only when purified human complement components were used to form erythrocyte-antibody-C3 immune complexes but was not detected when whole human serum was used as the source of complement. No IgM cell receptor was identified. Thus, with respect to membrane receptors, alveolar macrophages resemble peripheral blood monocytes. These studies in addition emphasize the importance of using a variety of immune reagents, especially the use of human reagents, to determine correctly these cell receptors.

Animals↗
PubMed1975

Clearances of complement components, C3 proactivator and other serum proteins in chronic membranoproliferative glomerulonephritis (CMPGN).

In chronic membranoproliferative glomerulonephritis (CMPGN) the activation of the complement system through the properdin pathway plays an important role. The clearance of complement components and of the C3-proactivator (C3-PA) have been determined in 18 patients. Hemolytically active C5, C6, C7 and C3-PA were detected in the urine for the first time. The clearances of the complement components did not correlate with the clearances of other serum proteins with similar molecular weights. The specificities of the single complement components in the urine were tested by specific complement inhibitors such as hydrazine, KSCN, and the C4-inactivating factor.

Adolescent↗