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At least 37 records · Page 2Linked to original sources
PubMed1977

Hereditary deficiency of the third component of complement in a child with fever, skin rash, and arthralgias: response to transfusion of whole blood.

A previously well 34-month-old male presenting with fever, skin rash, and arthralgias was found to lack C3 by immunochemical (undetectable) and hemolytic (1% normal) assays. No infectious agent could be demonstrated. Protein levels of Clq. C4, C5, properdin, and C3b-INA and hemolytic activities of complement components C1 to C9 except C3 were normal or elevated; total hemolytic complement activity was 13% of normal and was reconstituted by purified C3. Properdin factor B was 702 (normal 175 to 275) mug/ml, and was not cleaver upon addition of zymosan or cobra venom factor. The serum had normal immune adherence activity, but was deficient in ability to opsonize Candida albicans for uptake and Escherichia coli for killing by neurophils, generate neutrophil chemotactic factors and inhibit the growth of E. coli; these activities were restored by purified C3. A transfusion of 320 ml 1-hour-old normal whole blood on the fifty-second day resulted in transitory elevation of the C3 level to 25 mg/dl with a fall-off (approximately 2 1/2% per hour) to undetectable levels by 69 hours; it was followed by disappearance of the skin rash and arthralgias and return to normal of the previously elevated temperature and CRP levels. C3 levels in family members (seven of 24 half-normal), lack of anti-C3 activity, normal C3b-INA levels and a normal rate of catabolism of transfused C3 indicated that the deficiency was inherited with autosomal codominance and involved decreased synthesis of C3. Thus, this child is a unique individual with inherited C3 deficiency presenting with absence of repeated infections, whose symptoms of fever, skin rash, and arthralgia were abated by whole blood transfusion.

Blood Transfusion↗
PubMed1979

Idiopathic rapidly progressive glomerulonephritis with C3 nephritic factor and hypocomplementemia.

A 7-year-old boy with mild renal failure and signs and symptoms of acute poststreptococcal glomerulonephritis including severe hypocomplementemia had, by renal biopsy, numerous crescents but no deposits in the glomerular capillary loops. Instead, deposits identical in location and composition to those described for children with idiopathic rapidly progressive glomerulonephritis were present. The severe hypocomplementemia was found to be due to high levels of C3 nephritic factor; niether nephritic factor nor hypocomplementemia has been reported in rapidly progressive glomerulonephritis of the idiopathic type. Following prompt therapy with methylprednisolone intravenously, serologic abnormalities disappeared and renal function greatly improved, but a later biopsy showed 50% of the glomeruli obliterated by scarring. The case is of importance not only in indicating that severe hypocomplementemia does not rule out idiopathic rapidly progressive glomerulonephritis but also in adding to the list of diseases in which nephritic factor can be found.

Antigen-Antibody Complex↗
PubMed1975

Effect of staphylococcal protein A on complement-potentiated neutralization of herpes simplex virus and immune lysis of virus-infected cells.

Interaction of staphylococcal protein A (SPA) with human serum depressed the ability of such serum to neutralize herpes simpled virus (HSV)-antibody labialis. SPA-induced depression of serum-dependent virus neutralization appeared to be due to consumption of complement by SPA. In addition, SPA attached to antibody-treated, HSV-infected cells and inhibited complement mediated immune cytolysis. The amount of inhibition obtained depended upon the with the infected cells. The possible significance of SPA in the pathogenesis of viral disease complicated by secondary staphylococcal infection is discussed.

Animals↗
PubMed1977

Isolation and properties of complement-resistant strains of Escherichia coli K-12.

Several strains that were resistant to the bactericidal action of antibody and complement were isolated from Escherichia coli K-12 W3110/SM by selecting them through the medium containing antiserum and complement. They can be agglutinated by antiserum against the parent strain and showed similar immune adherence reactivity to the parent when sensitized with this antiserum. Few differences were found in the compositions of phospholipids and proteins between both inner and outer membranes of these strains and those of the parent. However, there were fewer short-chain and more long-chain fatty acids in these strains than in the parent. It was also found that unsaturated fatty acide decreased and saturated and cyclopropanoic acids increased in phosphatidylethanolamine and phosphatidylglycerol in both inner and outer membranes of one of these strains when compared with those from the parent. Therefore, the resistance of these strains to the complement-mediated bactericidal action was considered to be due to the rigidity of their membrane structures which might repel the insertion of membrane-attack complement complex C5b-9, although they could fix the earlier complement components up to the step of the formation of C4b,2a,3b complex enzyme.

Bacterial Proteins↗
PubMed1979

Role of complement in the expression of delayed-type hypersensitivity in rats: studies with cobra venom factor.

The hypothesis was tested that delayed-type hypersensitivity (DTH) to the complement-activating bacterium Listeria monocytogenes is initiated by complement-derived mediators that attract sensitized lymphocytes to reaction sites. To this end DTH and acquired resistance to L. monocytogenes were measured in rats injected with cobra venom factor, a potent inactivator of C3. Treatment with cobra venom factor reduced the hemolytic power of serum to less than 0.5% of the control value. Such decomplemented animals expressed both DTH and antimicrobial resistance, although expression of DTH was reduced (ca. 50%) when compared with complement-sufficient controls. The observed depression of DTH in cobra venom factor-treated rats was associated with a reduction in the number of recently activated lymphocytes (lymphoblasts) and macrophages that accumulated in DTH reaction sites. The above findings are explained, in part, by inhibition of inflammation during the early postinduction period. Supporting evidence came from measurements of labeled lymphoblast sequestration in saline injection sites and the slower accumulation of macrophages in nitrocellulose filters that were implanted subcutaneously in complement-depleted rats. The ability of cobra venom factor-treated rats to express DTH and protect themselves against a Listeria challenge seems to exclude C3-dependent factors as essential mediators in the attraction of antigen-reactive lymphocytes to reaction sites.

Complement Activation↗
PubMed1975

[Local Schwartzman phenomenon in axenic rabbits].

Local Schwartzman phenomenon was produced by coli-endotoxin in all the germfree rabbits tested (11 in all) at the age of 102 to 135 days. Any kinds of natural antibodies were not detected in sera of the rabbits, which in fact were found to be agammaglobulinaemic in most cases, as revealed by immunoelectrophoresis. These facts suggested that the germfree rabbits utilized here had not been sensitized to bacterial endotoxins. From the results obtained here, it may be concluded that the existence of hypersensitivity to endotoxin is not necessary to the production of local Schwartzman phenomenon by bacterial endotoxin.

Animals↗
PubMed1975

Complement biosynthesis in vitro by rat hepatoma cell strains.

Four separate rat hepatoma strains were examined for their capacity to synthesize complement (C). None of the strains synthesized detectable amounts of the first components (C-1), and only one strain (7800C-1) produced the fourth component (C4). However, each of the strains synthesized significant amounts of biologically active C-2 and C-3. Three of the four strains also produced C-5 and the natural inhibitor of C-1 (C1 INH). Two control rat cell strains (fibroblast and pituitary) did not synthesize any detectable C components. Production of C, studied extensively in 7800C-1 and H-4, was reversibly inhibited by cycloheximide (2 mug/ml) and [ 14-C ] amino acids were incorporated into C-2, C-3, and C-1 INH. As assessed by gel filtration, the elution positions of the C components synthesized by the cells in culture were similar to those of the corresponding proteins in normal rat serum. Hydrocortisone (10-6 to 10-7 M) stimulated the production of C-3 by H-4 but C-2 and C-5 production were not affected. These C-producing hepatoma cells may prove useful for studies of the control of C biosynthesis.

Animals↗
PubMed1976

C1 and human platelets. III. Role of C1 subcomponents in platelet aggregation induced by aggregated IgG.

Studies have been performed with platelets using C1 haemolytic assays and platelet aggregation induced by anti-C1q, anti-C1s and aggregated IgG in the presence of C1 subcomponents C1q, C1r and C1s. C1q was removed by EDTA or modified by collagenase from human platelets while after the same treatment C1s remained bound to the platelets. EDTA treated platelets were no longer aggregated by aggregated IgG. The addition of C1q restored the reactivity of the platelets to aggregated IgG while the addition of C1r or C1s was without effect. Furthermore, the addition of C1r or C1s to C1q inhibited the action of C1q in platelet aggregation induced by IgG.The possible association between the different C1 subcomponents and human platelets is discussed.

Complement C1↗
PubMed1977

[Immunologic reactivity of patients with acute leukemia].

In sera of patients with acute leucosis the authors have determined antibodies to alpha-toxin, streptolysin-O, the complement, lysosyme. B-lysins and C-reactive protein. It was found that the indices of immune reactivity in patients with acute leucosis are dependent on a morphological variant of the disease, the duration of the conducted therapy and presence of complications. The most high immunity indices in patients with acute leucosis were observed in a primary active stage of the disease and during the period of remission. Considerable reduction of the immunity was noted in the terminal stage of the disease.

Adult↗
PubMed1978

Antibasement membrane disease. II. Mechanism of glomerular injury in an accelerated model of Masugi nephritis.

Rabbits were given injections of preformed complexes of purified goat antirabbit glomerular basement membrane antibody and rabbit antigoat immunoglobulin. When the animals were killed 24 hours later, examination of their kidneys revealed diffuse glomerulonephritis with widespread areas of localized loop necrosis, associated with extensive accumulations of polymorphonuclear leukocytes. By electron microscopy, accumulations of polymorphonuclear leukocytes in various degrees of disintegration were associated with areas of the basement membrane that appeared to be losing their structural integrity, suggesting that the damage to the membrane was brought about by the action of lysosomal enzymes. Reduction of the number of circulating polymorphonuclear leukocytes by pretreatment of the animals with nitrogen mustard completely prevented the lesions. Reduction of circulating complement levels by pretreatment of the animals with cobra venom factor prevented the occurrence of localized necrosis but allowed the development of the diffuse lesion.

Animals↗