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PubMed1979

The role of Staphylococcus aureus cell-wall peptidoglycan, teichoic acid and protein A in the processes of complement activation and opsonization.

The role of cell-wall peptidoglycan, teichoic acid and protein A in the processes of Staphylococcus aureus complement activation and opsonization was investigated. CH50 consumption studies reveal that, although all cell-surface fractions were capable of activating the classical C pathway, only peptidoglycan consumed C via the alternative pathway. Using a quantitative immunofluorescence assay, peptidoglycan was shown to bind C3 molecules via the classical as well as via the alternative C pathway and in the absence of IgG and IgA class antibodies. C activation via the classical and the alternative pathway could be distinguished by kinetic analysis. By comparing the rates of staphylococcal C consumption, C3 fixation and opsonization it was found that the CH50 consumption assay is a relatively insensitive method and may yield results that do not necessarily reflect the process of bacterial opsonization.

Complement Activation↗
PubMed1975

The influence of C3b inactivator (KAF) concentration on the ability of serum to support complement activation.

Minor elevation of the concentration of the C3b inactivator (KAF) in whole serum (by 15-25%) markedly inhibits the capacity of the serum to support complement activation by inulin, aggregated IgG and by low concentrations of CVF. However, there was no effect when large concentrations of CVF were used nor was the spontaneous ageing of C3 slowed by increased KAF concentrations. These findings show that the activity of the C3b feedback cycle can be reduced by raising the KAF concentration above physiological levels. This finding may provide a mechanism for damping down complement activation locally in vivo. It seems that the spontaneous ageing of C3 in vitro does not involve a KAF-inhibitable step and therefore cannot be involved to explain the 'C3 tickover' in vitro.

Animals↗
PubMed1984

C3-independent immune haemolysis: haemolysis of EAC14oxy2 cells by C5-C9 without participation of C3.

C3-independent immune haemolysis was studied using EAC14oxy2 cells and purified C5, C6, C7, C8 and C9. We have found that EAC14oxy2 cells were lysed by C5-C9 and that haemolysis occurs, even after pretreatment of the cells and the C5-C9 preparation with anti-C3. This indicates that EAC14oxy2 can be lysed by C5-C9 without any participation of C3. In contrast, EAC1 and EAC14 cells are not lysed by C5-C9, suggesting that our C5-C9 preparation lacks activated complement components, such as C3bBb, C5b6 or C(56)a. Based on our study of the haemolysis of EAC14oxy2, we have determined that: (i) EAC14oxy2 cells are lysed by a preparation of C5, C6, C7, C8 and C9, but no lysis occurs when any one of these complement is absent, (ii) for significant haemolysis of EAC14oxy2, a higher concentration of C5 is necessary as compared to the C5 requirement when haemolysis occurs in the presence of C3, (iii) the degree of haemolysis is linearly related to the concentration of C5 and does not reach a plateau, despite the addition of as much as 3,200 U of C5, and (iv) the degree of haemolysis is linearly related to the concentration of cell bound C42. These observations suggest that, in the absence of C3, the C3 convertase C42 can activate C5 directly, resulting in the formation of the membrane attack complex, C5b-9.

Complement C2↗
PubMed1983

Immunogenetics of rheumatoid arthritis.

There is overwhelming evidence that Rheumatoid Arthritis (RA) is under genetic influence, but the mechanisms are unclear. Many studies have implicated HLA-DRA as an important marker for disease susceptibility, though this is not the case in all racial groups. Analysis of familial RA has shown a marked restriction in allelic combinations or supratypes. Mapping of the MHC by complement allotyping has further emphasised the relatively limited number of supratypes associated with RA. Disease associated supratypes may also serve as markers for complications induced by drugs such as D-penicillamine, and be shared by other diseases such as Type I Diabetes. That supratypes may have important biological functions is drawn from studies in complement C2 deficiency and 21-hydroxylase deficiency. Examination of supratypes should allow a more direct approach in understanding the pathogenetic mechanisms in RA, and the role of other markers outside the MHC.

Adult↗
PubMed1983

Effects of particulate beta-1,3 glucan on human, rat, and guinea pig complement activity.

Particulate glucan, a beta-1,3-linked polyglucose derived from Saccharomyces cerevisiae, has been demonstrated to have a wide range of immunopotentiating effects. Glucan administration is associated with the modification of a variety of experimentally induced infectious disease states as well as the inhibition of growth of implantable and spontaneous tumors. The present study was designed to evaluate the effect of glucan upon activation of the complement system in rats and guinea pigs. Additional studies were performed to determine the in vitro activating effect of glucan and zymosan on complement activity of human serum. Glucan activated both the classical pathway of normal human sera and the alternate pathways in C2hu-deficient sera in vitro releasing anaphylatoxins such as C3a. The intravenous injection of glucan activated the alternate pathway of guinea pig plasma. The influence of glucan on complement depletion induced by cobra venom factor (CVF) was also ascertained. Complement activation by glucan may contribute, in part, to the enhanced resistance of the host against tumor growth as well as infectious episodes.

Animals↗