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PubMed1986

Determination of anaphylatoxin concentrations in suction blisters in patients with psoriasis.

Concentrations of C3a and C4a anaphylatoxins in suction blister fluids were determined by radioimmunoassay in patients with psoriasis and normal controls. Comparison of anaphylatoxin levels between serum samples and blister contents in the same subjects revealed that the levels of both C3a and C4a anaphylatoxins were significantly higher in the former than the latter even in those raised on normal skin, suggesting that the classic complement pathway is activated during suction procedure. Therefore we cannot regard suction blister fluid to be simply representative of undisturbed interstitial tissue fluid as far as the complement system is concerned. There was no difference in anaphylatoxin levels between those from uninvolved skin of psoriatic patients and those from normal controls. However, significantly high anaphylatoxin levels were noted in fluids of suction blisters raised on lesional skin as compared with those produced on uninvolved skin in psoriatic patients.

Adolescent↗
PubMed1976

Complement and the clinician.

The estimation of complement in serum, and in other body fluids, particularly synovial fluid, now has an established place in the assessment, prognosis and response to treatment of those diseases associated with immunological phenomena. Some knowledge of the complement sequence itself, the patterns characteristic of various disease processes and the interacting factors which may affect the levels of the various components have been summarised. Disease states closely resembling lupus erythematosus have been associated with genetically determined deficiencies of classic pathway components and deficiencies of terminal sequence components may lead to severe recurrent infections.

Collagen Diseases↗
PubMed1985

Increased anaphylatoxins (C3a and C4a) in psoriatic sera.

We measured C3a and C4a anaphylatoxins in the serum of 56 psoriatic patients and 36 healthy control subjects by radioimmunoassay in order to clarify the mechanism of complement activation occurring in psoriatic lesions. Whereas a small amount of anaphylatoxins were demonstrable even in the sera of healthy adults, the serum concentrations of C3a and C4a anaphylatoxins were significantly higher in psoriatic patients than those in non-psoriatic controls. The increased serum anaphylatoxin levels did not correlate well with either the extent or the activity of the skin lesions, but a comparison of anaphylatoxin levels in 10 patients before and after successful treatment of skin lesions showed that the serum anaphylatoxin levels decreased with improvement of the skin lesions. Our results suggest that complement activation takes place in psoriatic patients chiefly via the classical pathway.

Adolescent↗
PubMed1986

Demonstration of anaphylatoxins C3a, C4a and C5a in the scales of psoriasis and inflammatory pustular dermatoses.

Complement components C3a, C4a and C5a were assayed in corneal scale extracts from psoriasis and other dermatoses characterized by sterile subcorneal pustules, using radioimmunoassay. Larger amounts were detected in psoriasis and related pustular dermatoses than in extracts of non-inflammatory stratum corneum. It is concluded that complement is activated via the classical pathway and releases the neutrophil chemotactic fragment C5a.

Anaphylatoxins↗
PubMed2004

The inflammatory response in mild and in severe psoriasis.

BACKGROUND: Psoriasis is a chronic and recurrent inflammatory skin disease. The inflammatory response represents a fundamental ability of the organism to protect itself from infectious agents and from injury. OBJECTIVES: To evaluate the inflammatory response in mild and in severe psoriasis, to evaluate the endogenous systems counterbalancing the deleterious effects of the inflammation products, and to establish values of prognostic significance. METHODS: The study was performed in a control group (n = 40) and in 60 patients with psoriasis vulgaris, half presenting with mild psoriasis, and the other half with severe psoriasis. We evaluated total and differential leucocyte count; elastase, lactoferrin and lipid peroxidation as markers of neutrophil activation; total plasma antioxidant capacity (TAS), transferrin, ceruloplasmin, alpha(1)-antitrypsin and alpha(2)-macroglobulin as markers of the endogenous antioxidant and antiprotease systems; and fibrinogen, erythrocyte sedimentation rate, C-reactive protein (CRP), haptoglobin, C3 and C4 complement proteins as markers of inflammation. RESULTS: Our data suggested that psoriasis is an inflammatory condition in which neutrophils seem to play a crucial role by contributing to the development of oxidative and proteolytic stress. The worsening of the disease seemed to be linked to the enhancement of the inflammatory response and of the imbalance between neutrophil activation products and their inhibitors. CONCLUSIONS: We propose values for elastase, CRP, elastase/alpha(2)-macroglobulin, elastase/alpha(1)-antitrypsin, thiobarbituric acid/TAS and elastase/neutrophil ratios with prognostic significance for the worsening of psoriasis.

Adult↗
PubMed1975

Red cell destruction in vivo by low concentrations of IgG anti-A.

Red cells coated with as little as 0.3-0.5 mug anti-A/ML cells were found to agglutinate if mixed with plasma and rocked on a tile, whereas the minimum amount of IgG anti-Rh required for agglutination under these conditions was about 50 mug antibody/ml cells. Complement-binding by red cells coated with IgG anti-A could be demonstrated only when the amount of antibody on the cells was at least 14 mug antibody/ml cells. Since in ABO haemolytic disease the amount of antibody on the cells is frequently less than 0.6 mug/ml cells, it seems that red cell destruction in this syndrome is not due to the activation of complement but may be due to the sequestration of agglutinated cells. A few experiments are described in which the survival in vivo of small amounts of agglutinated cells was studied. Reasons are given for considering that such experiments fail to mimic the conditions prevailing in ABO haemolytic disease.

ABO Blood-Group System↗
PubMed1985

Effect of complement on the viscoelastic properties of human erythrocyte membrane.

Using the micropipette technique, we examined the viscoelastic properties of the red blood cell (RBC) membrane which had been strongly coated with various components of complement (primary C3b, C3d, C4b, C4d) in vitro. The membrane elastic modulus (E), the viscosity index of the initial rapid phase of deformation (eta D1), the viscosity of the later slow phase of deformation (eta D2) and the viscosity of the recovery phase (eta R) were determined. Compared to control non-complement coated RBCs, RBCs coated with C3d, either alone or with other complement components, showed significant increase in the values for elasticity and viscosities. Thus C3d fixation resulted in decreased membrane deformability. Changes in membrane viscoelasticity due to bound C3d were not enhanced by bound C4b, C4d, C5, factor Bb or p; presence on RBC membrane of the latter two complement components may partially reverse the effect of C3d fixation. Lipid fluidity of RBC membrane, examined by fluorescence depolarization, increased with fixation of all complement components except C5. These complement-induced changes in membrane viscoelastic properties have potential pathophysiological and clinical implications. The data suggest that extravascular sequestration of human RBCs may be explained in part by increased membrane rigidity resulting from C3d fixation.

Complement C3↗
PubMed1988

Protein S and C4b-binding protein in fetal and neonatal blood.

The levels of protein C, free protein S, C4b-binding protein and the distribution of total protein S between a free form and a conjugated form with C4b-binding protein, were measured in fetuses between 15 and 35 weeks of gestation, in newborns and in maternal blood throughout pregnancy. Fetal and newborn umbilical blood samples were obtained by cordocentesis; in the case of newborns, immediately after delivery. C4b-binding protein was detected in five out of seven newborns and in only three out of 20 fetuses. The fetuses (21, 24, 29 weeks, respectively) whose blood contained C4b-binding protein (10%, 29%, 12% of adult level, respectively), did not survive: the possible cause of death for one was given as viral infection; all three were severely deformed. Only free protein S was detected in fetal blood and the mean value was 40%. By contrast, the mean levels of protein C in the fetuses increased from 11% to 15.5% of adult levels with advancing gestation. We conclude that the relatively high levels of free protein S in fetal blood may contribute to its non-coagulability and compensate for the low protein C levels.

Carrier Proteins↗
PubMed1989

A new case of 'type II' inherited protein S deficiency.

Protein S inherited deficiency is associated with high risk of recurrent venous thrombotic disease (Broekmans et al, 1985a, b). Protein S exists as two forms in plasma, either free and functionally active or complexed with C4b-binding protein (C4b BP) and inactive (Dahlbäck & Stenflo, 1981). We report here the case of a 26-year-old woman and her brother, 28 years old, both suffering from recurrent venous thrombosis since the age of 20, diagnosed as severe protein S deficiency according to the following data: free protein S: 2.5-3% by ELISA, undetectable by electroimmunodiffusion (EID); total protein S: 13-16% by ELISA, 21-18% by EID, C4b BP: normal levels. Crossed immunoelectrophoresis using anti-protein S antibodies revealed only traces of protein S associated with C4b BP and no free protein S. All these assays were performed in the absence of any anticoagulant therapy. Among the investigated relatives, less severe protein S deficiency was observed in three children of the propositus: total protein S levels ranging from 41% to 50% (EID), 40-53% (ELISA); free protein S levels ranging from 16% to 18% (EID), 10-12% (ELISA); normal C4b BP levels. Crossed immunoelectrophoresis revealed traces of free protein S but a significant amount of protein S associated with C4b BP. From these results, we consider, according to Comp's classification (Comp et al, 1986a), that the propositus and her brother are the second case of protein S deficiency type II to be reported in the literature while her children belong to the type I category.

Adult↗
PubMed1977

Haemostatic and complement changes in a family with 'allergic' disorders.

A family with allergic manifestations, haemostatic disturbances, total absence of haemolytic activity of the complement system and low IgG levels is described. It is suggested that this functional abnormality of the complement system and the decreased level of immunoglobulin G may be due to immune complex reactions.

Adolescent↗
PubMed1991

Vascular deposition of complement-split products in kidney allografts with cell-mediated rejection.

Complement activation in 73 renal transplant biopsies was investigated by indirect immunoperoxidase staining using MoAbs reactive with complement-split products. Intense deposition of complement fragments C4d and C3d in peritubular capillaries, indicating activation of the classical pathway, could be detected in the majority of transplanted kidneys with cell-mediated rejections. Abundant deposition of complement-split products was observed in 22 early biopsies from patients with high 'immunological risk' (i.e. previous, rejected transplants and/or circulating antibodies against HLA-antigens). Despite negative results in the crossmatch before transplantation and paucity of immunoglobulins in transplant biopsies, antibodies directed against endothelial cell antigens should be considered as a possible cause of classical complement activation.

Antibodies, Monoclonal↗
PubMed1991

Characterization of anti-endothelial cell antibodies in systemic lupus erythematosus (SLE).

IgG anti-endothelial antibodies (AEA), as measured by ELISA or immunoblotting technique could be detected in serum samples of 56 out of 64 patients with SLE (88%) and mainly occurred in monomeric form. AEA were not cell specific, because the binding reactivity was absorbed partially by both fibroblasts and peripheral blood mononuclear cells. No correlation was found between the presence of AEA and anti-nuclear antibodies. Immunoblotting revealed reactivity of AEA against endothelial antigens ranging in size from 15 to 200 kD. AEA titres were significantly higher in patients with joint or skin abnormalities, compared with patients without these abnormalities. A significant correlation was found between nephritis in SLE and the presence of AEA reactivity against endothelial membrane antigens of 38, 41 and 150 kD. These data show that the pattern of AEA reactivity in serum of SLE patients is heterogeneous, and suggest that AEA against a limited number of antigens may be involved in the pathogenesis of nephritis in SLE.

Antibodies, Anti-Idiotypic↗
PubMed1992

Functionally active complement is present in human ovarian follicular fluid and can be activated by seminal plasma.

Human ovarian preovulatory follicular fluids (FF) from 10 women were analysed for their complement contents. Functionally active complement was detected in all the fluids studied in amounts similar to those present in normal human serum. Pooled FF was challenged by seminal plasma in order to determine whether seminal plasma could activate FF complement, the pattern of such an activation and the possible consequences on the reproductive function. FF complement activation occurred during the incubation with seminal plasma with features including alternative pathway activation, factor B and C3 conversion and reduction in total haemolytic complement, as well as an inhibition by seminal plasma of the FF complement response to a new activating challenge. Possible consequences for fertilization, implantation of a fertilized ovum and local defence mechanisms against viruses and bacteria are discussed.

Complement Activation↗