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PubMed1981

Complement activation in nonsystemic glomerular diseases in children.

All forms of glomerulonephritis (GN) in man seem to be immunologically mediated and the complement system appears as one of the most important mediators of renal injury. The study of complement activation is therefore of great help in the identification of the immunopathogenic process involved in the various types of glomerular diseases. After a review of the molecular events of complement activation and the methods used to study the complement system in man, we will attempt to summarize current knowledge concerning complement in nonsystemic glomerular diseases frequently encountered in children. The terms used are those descriptive of glomerular morphology as defined either by light microscopy and electron microscopy (endocapillary-proliferative GN with humps, extramembranous GN, membranoproliferative GN) or by immunofluorescent microscopy (mesangial IgA GN).

Basement Membrane↗
PubMed1982

Restricted deposition of C3 on M+ group A streptococci: correlation with resistance to phagocytosis.

In this report, the mechanism of resistance to phagocytosis by group A streptococci and the participation of M protein in this process were studied. A quantitative fluorometric immunoassay was used to determine the amount of the opsonic third component of complement, C3, fixed by group A streptococci in the presence and absence of M protein. In the absence of M protein, phagocytosis was found to be dependent on the amount of C3 fixed. However, when M protein was present, the streptococci still bound sufficient C3 to have promoted phagocytosis, yet none was observed. Further investigation using immunofluorescent microscopy demonstrated that the C3 fixed to M+ chains was confined to dense patches, interspaced by areas devoid of detectable C3. This uneven distribution of C3 was dependent on the presence of a trypsin-sensitive structure; most likely the M protein. The significance of this restricted C3 deposition with respect to resistance to phagocytosis by group A streptococci is discussed.

Animals↗
PubMedDate not supplied

[Genetics of complement: recent aspects (author's transl)].

Genetic deficiencies of complement proteins are now more often recognized and analysed more precisely because the structure of the different complement proteins is better known. Partial defects may be detected in some components by the combined utilization of titration techniques, polymorphism studies and linkage analyses. The partial deficiency in C4 seems to be the most frequent protein deficiency in the human. The complement markers on the short arm of the sixth chromosome in man (BF, C2, C4A and C4B) are located in close proximity to the HLA-D/DR region. The combined study of the complement and HLA markers will probably allow the fine structure of the HLA region to be better defined. The association of some diseases with HLA types will probably also be better specified by the definition of associations not only with HLA-B or HLA-D types but also with the BF, C2 and C4 types.

Animals↗
PubMedDate not supplied

[The manifestation of functional heterogeneity of the peptidoglycans in opsonophagocytic reactions].

The peptidoglycan activity of Staphylococcus aureus CCM 885 and Bifidobacterium bifidum 1 was studied in the opsonophagocytic system on the basis of the luminol-dependent chemiluminescence of human neutrophils. B. bifidum peptidoglycan was more active in direct interaction with neutrophils. After treatment with normal human serum S. aureus peptidoglycan showed more pronounced neutrophil-stimulating properties. This phenomenon was in accord with a higher content of IgG antibodies to S. aureus peptidoglycan, as well as with its capacity for the classical direct activation of the complement. Moreover, in reactions with S. aureus peptidoglycan "minor" opsonins, independent of antibodies and complement, were detected. B. bifidum peptidoglycan did not activate the complement, could not be opsonized with the serum having no specific antibodies and did not react with "minor" opsonins.

Bifidobacterium↗
PubMed1996

In vitro anti-complementary activity of flavonoids from olive (Olea europaea L.) leaves.

From extracts of olive (Olea europaea L., Oleaceae) leaves showing anti-complementary activity, the flavonoids apigenin, apigenin-4'-O-rhamnosylglucoside, apigenin-7-O-glucoside, luteolin, luteolin-4'-O-glucoside, luteolin-7-O-glucoside, chrysoeriol, chrysoeriol-7-O-glucoside and quercetin-3-O-rhamnoside were isolated. Major isolated constituents strongly inhibited the classical pathway of the complement system.

Complement Inactivator Proteins↗
PubMed1998

Therapeutic inhibition of the complement system.

The use of powerful methodologies in molecular biology, biochemistry, and physiology in the last 2 decades had led to impressive progress in our understanding of the mechanisms of complement activation and its role as either a protective or a pathogenic factor in human disease. With respect to disease pathogenesis, the complexity of the complement cascade provides opportunities for several different therapeutic targets within the complement pathways. More than a century after complement was first described, we are about to witness in the near future the availability of a variety of complement inhibitors for specific therapies. Progress in the area of xenotransplantation has been substantial, but formidable obstacles remain to selective inhibition of the factors that block successful clinical xenotransplantation. Bispecific antibodies, designed to enhance rather than inhibit existing complement pathways, hold strong promise for the clearance of viral and bacterial pathogens from the circulation.

Animals↗
PubMed1999

Anti-ICAM-1 monoclonal antibody R6.5 (Enlimomab) promotes activation of neutrophils in whole blood.

R6.5 (BIRR-1, Enlimomab), a murine IgG2a mAb to the human ICAM-1, inhibits leukocyte adhesion to the vascular endothelium, thereby decreasing leukocyte extravasation and inflammatory tissue injury. In initial clinical trials, R6.5 proved to be beneficial in reducing both disease activity in refractory rheumatoid arthritis and the incidence of acute rejection after kidney and liver allograft transplantations. However, adverse effects such as fever, leukopenia, or cutaneous reactions were not infrequent. We studied the effects of R6.5 on neutrophil function in whole blood samples ex vivo. Surprisingly, at the concentrations achieved in clinical trials, R6. 5 activated neutrophilic granulocytes, as indicated by a significant increase in expression of the adhesion molecule beta2-integrin CD11b, a concurrent decrease in L-selectin expression, and an enhancement of the oxidative burst activity. Neutrophil activation was not exerted by an anti-ICAM-1 mAb of the IgG1 isotype, by isotype-matched, irrelevant anti-2-phenyloxazolone mAb, or by F(ab')2 fragments of R6.5. Neutrophil activation was completely inhibited by soluble complement receptor type 1. We conclude that in whole blood, R6.5 activates resting neutrophils in a complement-dependent manner. This finding can explain, at least in part, the side effects associated with R6.5 therapy.

Animals↗