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PubMed1993

Regulation of complement membrane attack complex formation in myocardial infarction.

Recent studies have suggested that the complement (C) system is involved in the development of tissue injury of myocardial infarction. As it is not known why the strictly controlled C system starts to react against autologous heart tissue, we have analyzed the expression of various membrane regulators of C (CR1, DAF, MCP, CD59, C8 binding protein) and the pattern of deposition of C components and plasma C regulators (C4b binding protein and vitronectin) in normal (n = 7) and infarcted (n = 13) human myocardium. In the infarcted myocardium deposits of the C membrane attack complex (MAC) were observed by immunofluorescence microscopy, and lesions resembling the transmembrane channels of MAC were detected by transmission electron microscopy. CD59 and C8 binding protein were strongly expressed by muscle cells of normal myocardial tissue. Little or no CR1, MCP, and DAF was observed on these cells. The assembly of MAC was accompanied by the deposition of vitronectin (S-protein) and C4b binding protein in the infarcted areas of myocardium. In accordance with our earlier results the expression of CD59 but not of C8 binding protein was clearly diminished in the lesions. The results show that C8 binding protein, vitronectin, and C4b binding protein do not prevent complement attack against the infarcted myocardium but rather become codeposited with the MAC. Ischemia-induced transformation of nonviable cells into complement activators, acquired loss of resistance to the MAC by shedding of CD59, and recruitment of multifunctional serum proteins by MAC could thus constitute a general process aimed at the clearance of injured tissue.

Aged↗
PubMed1995

Cryoglobulinaemias: a multi-centre study of the early clinical and laboratory manifestations of primary and secondary disease. GISC. Italian Group for the Study of Cryoglobulinaemias.

In a multi-centre retrospective study, we compared clinical and laboratory data in 913 patients with cryoglobulinaemias, divided as: (i) essential cryoglobulinaemias; (ii) cryoglobulinaemias secondary to connective tissue diseases (CTD), lymphoproliferative or other haematological diseases (LPD), chronic liver diseases (CLD), and 'other diseases'. Purpura was the commonest presenting feature in all groups and was more common in essential cryoglobulinaemias (p < 0.0001). Meltzer's triad (purpura, arthralgia, weakness) was less frequent, but similarly distributed. Renal involvement was randomly distributed. Neurological impairment was less frequent in cryoglobulinaemias secondary to CLD (p < 0.002). Raynaud's phenomenon, arthritis and sicca syndrome were more frequent in cryoglobulinaemias secondary to CTD. Essential cryoglobulinaemias had a significantly higher percentage of serum complement C4 < 8 mg/dl (p < 0.004), of detectable rheumatoid factor activity (p < 0.0002), and of type II cryoglobulins (p < 0.0001). Liver involvement was evident at presentation in 32.6% of essential cryoglobulinaemias, 27.1% of cryoglobulinaemias secondary to LPD and 12.2% of cryoglobulinaemias secondary to CTD. Antibodies to hepatitis B surface (HBsAg) and core (HBc) antigens were more frequent in cryoglobulinaemias secondary to CLD; anti-HBs antibodies were randomly distributed. Antibodies to hepatitis C (HCV) were tested for in 224 patients, and prevalence was high in all the groups, but lower in cryoglobulinaemias secondary to CTD (p < 0.0001). Type II and type III essential cryoglobulinaemias differed significantly in renal involvement (p < 0.0001), cryocrit > 3% (p < 0.0001), C4 < 15 mg/dl (p < 0.001), HBsAg prevalence (p < 0.01) and purpura (p < 0.05). Despite the high prevalence of HCV markers in all groups, the role of HCV in essential cryoglobulinaemia is not well defined; HBV seems to play only a marginal role.

Adolescent↗
PubMed1995

[Comparison of complement activation between tuberculous and malignant pleuritis].

Complement activation products in pleural effusions were studied to clarify the causes of tuberculous and malignant pleuritis. Pleural SC5b-9, an activation product of complement common pathway, was significantly higher in tuberculous effusions than in malignant ones. In the tuberculous effusions, the levels of SC5b-9 and LDH (a marker of tissue damage) were significantly correlated, but in the malignant effusions these two values were not correlated. In the tuberculous effusions, SC5b-9 and Bb values were significantly correlated, but SC5b-9 and C4d were not, and nor were SC5b-9 and immune complex. In the malignant effusions, SC5b-9 and Bb values were low and were not significantly correlated. These results suggest that complement activation plays a significant role in tuberculous pleuritis, but not in malignant pleuritis.

Antigen-Antibody Complex↗
PubMed1975

Deficiencies of the complement system in man.

Deficiencies of components of the complement system in man are described. Clq was reconstituted in patients with severe combined immunodeficiency after bone marrow transplantation. Clr deficiency is associated with vascular disease and upper respiratory infections. Reconstitution of complement occurred in one patient with Clr deficiency after kidney transplantation. Our C2-deficient patient who developed systemic lupus erythematosus had elevated levels of C3. Following blood transfusion, ie by providing C2, dramatic activation of complement occurred in vivo.

Blood Bactericidal Activity↗
PubMed1994

Complement activation in platelet concentrates is surface-dependent and modulated by the platelets.

Activation of platelets during storage may contribute to the loss of function and viability known as the platelet storage lesion. We investigated the role of complement activation as a possible mediator of the platelet storage lesion. We studied platelet bags stored up to 5 days under standard blood bank conditions and monitored the generation of several complement activation fragments from both the classical and alternative pathways. To assess the role of noncellular artificial surfaces in the activation of complement, parallel bags were prepared containing platelet-poor plasma. The levels of C4d and C3a increased steadily over time in storage, as did the level of the inactivated membrane attack complex SC5b-9. Generation of C4d, C5a, and SC5b-9 was greater in the absence of platelets than when platelets were present in the container. C5a levels in both groups were low and remained so during storage, suggesting that the C5a generated became surface associated. Using flow cytometry we detected C3 and C3a, but not C9, on the platelet surface. The percentage of C3-positive platelets peaked at the third day of storage; by day five platelet-associated C3 had declined. Decay accelerating factor expression on the platelet surface increased with time in storage and in parallel with CD63 expression. Based on the C4d levels, complement activation proceeded via the classical pathway; minimal generation of the alternative pathway activation fragment. Bb was seen in either the presence or absence of platelets. As an indirect measure of the activation of C1, the functional level of C1 esterase inhibitor (C1INH) was determined. C1INH levels declined over time in storage in bags containing only plasma; however, in the presence of platelets, the levels remained constant presumably because of release of C1INH from the alpha-granules of activated platelets.

Blood Platelets↗
PubMed1977

Immunosuppression of T lymphocyte function by fractionated serum from tumor-bearing mice.

Sera from mice with transplanted 3-methylcholantrene-induced tumors have been shown previously to inhibit the function of normal lymphoid cells. When chromatographed on Sephadex G-150, the fraction eluting with immunoglobulin has been shown to inhibit the proliferative response of normal spleen cells to concanavalin A and to inhibit the in vitro antibody response to a T-dependent antigen, but has a lesser effect on the antibody response to a T-independent antigen. This paper deals with studies on the mode of action of the serum factor. The immunoglobulin containing fraction of serum from tumor-bearing mice inhibited the in vitro generation of both allogeneic and syngeneic cytotoxic lymphocytes. Time course studies demonstrate that the serum fraction inhibits the generation of antibody-producing and cytotoxic lymphocytes if added during the first 2 days of a 5-day culture. Serum fractions added after day 2 had no effect on the in vitro response. The serum factor appears to inhibit the generation of specific T cell function during the proliferative stage of development but has no effect on the differentiation stage which leads to either antibody-producing cells or cytotoxic lymphocytes.

Chemical Precipitation↗
PubMed1993

[Complement analysis tests].

Although routine analysis of the complement system is rarely demanded, it is important from a diagnostical and therapeutical point of view to include the relevant tests when clinically required. Complement analysis should be performed when hereditary angioedema (C1 inhibitor deficiency) is suspected, and as part of investigation of patients with immunodeficiency (recurrent infections in childhood). Furthermore, complement analysis may be required in cases of recurrent systemic neisserial infections at any age, and to follow up certain autoimmune diseases. Only a few tests are available for routine purposes. These are reviewed briefly, with emphasis on collection and storage of samples prior to analysis. It is important that these guidelines be followed, to avoid misinterpretation of the results.

Angioedema↗
PubMed1993

Complement activation and immune complexes in juvenile rheumatoid arthritis.

We investigated the potential role of the complement system in juvenile rheumatoid arthritis (JRA) by examining plasma for levels of complement activation fragments C4d and Bb. We correlated findings with both disease activity and laboratory abnormalities, including immune complex (IC) levels. While there was a strong correlation between active disease and both C4d and Bb plasma levels in JRA, no strong correlations could be made between IC levels and complement activation products; weak associations were seen between complement activation fragments and erythrocyte sedimentation rate. Our data suggest that plasma complement activation is a concomitant of active disease in JRA; however, its role in the pathophysiology of JRA remains uncertain.

Antigen-Antibody Complex↗
PubMed1993

[A case of severe bronchospasm and laryngospasm after atracurium administration].

We present a case of severe intraoperative bronchospasm and laryngospasm, that happened after the administration of atracurium 0.5 mg/kg-1; this episode was very difficult to manage, in spite of a prompt bronchodilative treatment. This episode of bronchospasm happened again after extubation and it was so severe that it was necessary to intubate the patient quickly again. We administered bronchodilatative drugs again, and after half an hour it was possible to extubate the patient and to send him to the ward. He had no problems in the postoperative period. We carried on some investigations to evaluate the nature of this reaction: we measured the level of IgE, C3 and C4 complement factor during operation (one sample), in the first and second postoperative days. Moreover we did an intradermal test for all the drugs used during the operation. We concluded that it was an anaphylactoid reaction, sustained by atracurium.

Adult↗
PubMed1995

[Rheumatoid pericarditis: correlation with immunologic parameters].

In 35 patients with rheumatoid pericarditis the laboratory findings were compared with those of a group of 65 patients with rheumatoid arthritis without a pericardial exudate. The authors assessed the red cell sedimentation rate and serum levels of immunoglobulins G, M, A, semiquantitative values of the rheumatoid factor, circulating immunocomplexes, C3 and C4 complement components, the positivity of antinuclear antibodies and values of C-reactive protein. The authors found significantly elevated values of immunoglobulins M in patients with rheumatoid arthritis without a pericardial exudate. As regards the other investigated parameters the two compared groups did not differ.

Adult↗
PubMed1977

Inhibition of complement by mouse serum: selective inactivation of the fourth component of human complement.

Bound human C4b on EAC4 is rapidly inactivated in the presence of murine serum reagents. The functional characteristics of this inactivation suggest that it is probably caused by factor(s) homologous to human C3bI-C4bI: inactivation is temperature-dependent and occurs without concomitant consumption of the inactivator(s); loss of hemolytic function is associated with the cleavage of the bound C4b into C4c, which is released, and C4d, which is retained on the cell membrane. Murine serum reagents inhibit bound human C4b far more efficiently than C3b and may therefore be employed to selectively inhibit C4b.

Animals↗