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PubMed1979

Circulating immune complexes in acute uveitis: a possible association with the histocompatibility complex locus antigen B27.

39 patients with acute anterior uveitis were investigated for the presence of circulating immune complex (IC) and correlation with the major histocompatibility complex antigen B27 (HLA-B27). ICs were demonstrated by a number of techniques including rheumatoid factor, complement (C) activation, anticomplementary activity, cryoglobulins, inhibition of IgG-EA rosette formation and neutrophil chemotactic index (NCI) in plasma. ICs were most frequently detected in HLA-B27-negative patients. These results indicate that deposition of circulating ICs may be involved in the pathogenesis of acute anterior uveitis, especially in HLA-B27-negative patients.

Acute Disease↗
PubMed1980

Effect of aspirin on the complement system in vitro.

Aspirin (acetylsalicylic acid), ASA and sodium salicylate (NaSA) activate the complement system in vitro. The activation involves the components of the classical pathway. It is, however, antibody independent. Evidence for activation are (1) consumption of C and C component activities; (2) activation of C1 evidenced by release of C1s from the macromolecular complex, and (3) C3 and C5 conversion.

Aspirin↗
PubMed1980

Antibody-independent complement consumption by Micropolyspora faeni.

Micropolyspora faeni is an etiologic agent of hypersensitivity pneumonitis, a disease with an ill-defined mechanism of pathogenesis. Many reports have suggested an immunologic mechanism. A number of laboratories have demonstrated a nonantibody-mediated activation of the complement cascade. This study was undertaken to define the pathway of the complement consumption induced by M. faeni. We utilized an extract of M. faeni grown on synthetic media rather than the more common double dialysis extracts. Complement consumption by this extract was easily demonstrable in the absence of detectable antibody, but was inhibited by EDTA and MgEGTA. With the exception f C1, all of the early components of the classical pathway were markedly reduced following incubation of normal human serum with this extract. C1 was poorly consumed. In addition, factor B conversion to B was not inhibited by 10 mM MgEGTA suggests that the alternative pathway may also be affected. The generation of M. faeni-dependent chemotactic factor(s) from serum demonstrates that the complement cascade is being activated rather than inhibited.

Antibodies↗
PubMed1984

Complement components, complement activation, and acute phase response in systemic lupus erythematosus.

The investigation concerned 33 systemic lupus erythematosus (SLE) patients assigned to three groups representing mild SLE, more severe extra renal SLE, and SLE with significant renal involvement. In patients with extrarenal disease, the inflammatory plasma protein response was often pronounced during exacerbation, as evidenced by markedly increased concentrations of C-reactive protein (CRP), alpha 1-antichymotrypsin, alpha 1-antitrypsin, and orosomucoid. CRP responses were rare in patients with renal involvement, despite the increased concentrations of other acute-phase reactants in some of these patients. Superimposed bacterial infections were not clearly distinguished by raised CRP concentrations. The classical pathway of complement was activated in all patients during exacerbation, as indicated by increased concentrations of C1r-C1s-C1 inactivator complexes and C2a fragments. C1, C2, and probably also C3 activation varied according to the amounts of circulating C1q-binding immune complexes, as measured by solid-phase assay. Manifest hypocomplementemia was usually associated with glomerulonephritis. Participation of complement components in the inflammatory plasma protein response apparently counteracted the development of hypocomplementemia in many patients with extrarenal SLE. Circulating C3d was detected in all patients during exacerbation of renal disease and in most patients with severe extrarenal manifestations. Inverse relationships were found between immunochemical C2 concentrations and the percentage of cleaved C2 and between C3 and C3d. There was no appreciable consumption of factors B and D and properdin of the alternative pathway in the patients. High concentrations of factor D, a low molecular weight protein, were exclusively found in patients with renal involvement and could be ascribed to retention due to reduced glomerular filtration.

Antigen-Antibody Complex↗
PubMed1985

Complement anaphylatoxins in idiopathic mixed cryoglobulinemia.

Basophil activation, observed in patients with idiopathic mixed cryoglobulinemia, has been related to the complement anaphylatoxins C4a, C3a and C5a. In the present study the plasma levels of the complement anaphylatoxins have been evaluated in 21 patients affected with idiopathic mixed cryoglobulinemia. The plasma concentration of C3a desArg was significantly higher in the patients than in the healthy controls; conversely the plasma values of C4a desArg were significantly lower. C5a desArg was not detectable in plasma from any subject. The high plasma level of C3a desArg in our patients may suggest a role for C3a anaphylatoxin in 'in vivo' basophil activation. No correlation was found between the plasma concentrations of C3a desArg or C4a desArg, the amount of cryoprecipitate and the clinical activity of the disease.

Adult↗
PubMed1988

Studies on the formation of a unique cellular intermediate (EAC14256) from EAC142 and C56.

The binding reaction of C56 to EAC142 was studied. The following was observed: (1) C56 can bind to EAC142, without participation of C3 or C7, to form EAC14256; (2) the efficiency of EAC14256 formation from EAC142 and C56 depends highly on the ionic strength of the buffer; (3) EAC14256, generated from EAC142 and C56, decays spontaneously by elution of C56 into the medium and thus the reaction between C56 and EAC142 is reversible; (4) the receptor on EAC142 for C56 is C2 or C42 on the cell surface, and (5) the binding of C56 to C2 or C42 on cells is independent of the usual (C3-dependent) complement cascade activation. These observations, together with the results of our previous report, indicate that the binding of C56, generated from the activation of C5 by C42 (without C3), to EAC142 may be the initial step of membrane attack complex formation in C3-independent immune hemolysis.

Antibodies↗
PubMed1991

In vitro formation of complement activation products by lipopolysaccharide chemotypes of Salmonella minnesota.

We have applied immunoassays for complement activation products C4d, fragment Bb and the protein S-C5b-9 neoantigen (S-MAC) to assess activation of classical, alternative and terminal pathways, respectively, by lipopolysaccharides (LPS) from the smooth strain (SS) of Salmonella minnesota and the shallow rough (core) mutants R60, R345, R5 and R7. Incubations of sera (n = 6) with LPS generated small and insignificant quantities of Bb and S-MAC in the case of Rb, Rc and Rd chemotypes and slightly greater quantities with Ra. SS-LPS brought about significant (p = 0.01) increases in the formation of both Bb and S-MAC. No significant changes were observed in the concentration of C4d. Polymyxin B enhanced Bb and S-MAC production by SS-LPS, optimally at the lowest concentration of polymyxin B studied, 10 ng/ml. These data confirm and extend observations about complement activation by LPS and suggest that immunoassay may be useful in studying mechanisms of complement activation.

Adult↗
PubMed1990

Activation of the alternative pathway of complement in psoriatic lesional skin.

The complement system may play an important role in the inflammatory reaction of psoriasis. While the classical pathway of the complement has been shown to be activated in psoriasis, there have been few reports on the involvement of the alternative pathway in the inflammatory reactions in psoriasis. Complement fragments, C4d and Bb, are released at the time of the classical and alternative pathway activation, respectively. The presence of the C4d or Bb fragment, therefore, denotes a preceding complement activation through the classical and/or alternative pathway. In the present study, we have measured the levels of C4d and Bb in psoriatic scale extracts using enzyme immunoassay techniques. The scales of these dermatoses contained higher levels of C4d and Bb detectable by enzyme immunoassay than those in the stratum corneum of noninflammatory skin. These results suggest that the alternative as well as the classical pathway of complement are activated in psoriatic lesional skin.

Complement Activation↗
PubMed1989

Assessment of the activation pathways of the complement in psoriatic patients by use of complement fragment C4d and Bb measurements.

We have measured the complement fragment C4d and Bb levels in the plasma of 51 psoriatic patients and 54 normal controls. The C4d and Bb levels were not significantly elevated in the plasma of the psoriatic patients when compared with those of controls, except in patients with more than 60% skin involvement who exhibited an increase in Bb levels. C4d levels, however, did decrease slightly after successful treatment of psoriasis. Although these results suggest that the C4d and Bb levels partly reflect the complement activation in vivo, they do not seem to be suitable parameters to clarify the mechanism of complement activation in psoriasis.

Adolescent↗
PubMed1989

Alterations in the terminal complement pathway in leukopenic children with malignant diseases during episodes with evidence of infection.

A prospective study comprising 23 children under treatment with cytostatic drugs for malignant diseases was undertaken to search for complement abnormalities during episodes with evidence of infection. Eleven patients developed 17 episodes with fever (temperature greater than or equal to 38 degrees C) (n = 13) and/or increased concentration greater than or equal to 10 mg/l) of C-reactive protein (CRP) (n = 16). Complement factor C9 increased significantly (greater than or equal to 150%) in 12/13 of the events with fever, in 16/16 with increased CRP, and in 1 additional event with normal temperature and CRP concentration. The terminal complement complex (TCC) increased excessively (37.2 units/ml) parallel to a fall in C9 and S-protein in a single patient with a lethal septic shock, and was slightly increased (2.9 units/ml) in a 2nd case who was efficiently treated. These were also the only 2 cases with verified bacterial infections. We conclude that C9 is a valuable supplement to CRP for detection of events with probable infection and that TCC is increased only in severe infection and may be of prognostic importance.

Adolescent↗
PubMed1990

Two BF*F subtypes found by isoelectric focusing have restricted distributions in the Finnish MHC haplotypes.

The factor B (BF) polymorphism revealed by immunofixation of plasma samples is made up of more than 20 variants, of which 2 variants are common, S and F, 2 less common, F1 and S07, and the rest of the variants are very rare. In this work we have adapted a rapid method to subdivide the BF*F allele into *FA and *FB by IEF in nontoxic agarose gel. The FA subtype manifested as two major bands and FB as one band both in native and desialylated samples. *F1, *S and *S07 were shown as monomorphic proteins, but differ in their sensitivities to degradation caused by neuraminidase treatment. *FA and *FB showed restricted distributions among the HLA haplotypes of the homogenous Caucasoid Finnish population. *FA was positively associated with the haplotypes Cw3,Bw62,C4A3BQ0 (or A3B1) and *FB with the haplotypes A3,Cw4,B35,DR1,C4A3BQ0 (or A2BQ0, A3,2BQ0).

Alleles↗
PubMed1985

Increased plasma levels of the terminal complement complex in patients with evidence of complement activation.

The terminal C5b-9 complex of human complement has recently been described and quantified in normal human plasma by an enzyme-linked immunosorbent assay (ELISA). We collected EDTA plasma samples from 20 patients clinically suspected to have complement activation. The terminal complement complex (TCC) and C3d split products were measured. The TCC was increased in 8 patients, and 6 of these also had increased C3d values, whereas 4 patients had increased C3d and normal TCC values. Two different double-antibody assays were used to detect terminal pathway activation: the combination of anti-C6 and anti-C9 detecting only the whole complex, and the combination of anti-C6 and anti-C5 detecting intermediate complexes as well. There was a close correlation between the observations in these two assays, suggesting that in general the whole cascade including C9 is involved when the terminal pathway of complement is activated in vivo. Quantification of TCC in plasma is an important supplement to already established methods for the evaluation of complement activation in vivo.

Adult↗
PubMed1986

Biochemistry and biology of anaphylatoxins.

The molecular architecture of anaphylatoxins has been explored on several levels. Primary, secondary and tertiary structural parameters that dictate function of the C3a, C4a and C5a molecules are being elucidated with the aid of comparative sequence analyses, physical measurements and organic syntheses. Although C3a, C4a and C5a are biologically distinct mediators, as defined by their unique receptor systems, a common genetic origin is apparent from conserved features in their primary structures. Evidence is now available which suggests that similarities in the folding pattern of the anaphylatoxins may dictate a concensus conformation for each factor. We have learned from synthetic peptide studies that the binding (e.g. effector) site in anaphylatoxin molecules exists as a linear sequence contained in the C-terminal portion of the polypeptide. What is also evident is that a preferred conformation is defined for the binding site requiring a proper side chain orientation for optimal bioactivity. It is proposed that folding of the native structure stabilizes this conformation at the binding site. The binding site in C3a contains the essential residues LGLAR folded in an irregular or pseudo-beta-turn and stabilized by an adjacent alpha-helical segment. It is proposed that the alpha-helical segment influences orientation of the side chain residues in the 'binding site'. A similar model is evolving for C5a based on synthetic C5a peptides that express both spasmogenic and chemotactic activities. This helix turn model promises to be representative of an essential structural feature that determines anaphylatoxin activity. We believe that these models contribute significantly to our understanding of the molecular relationships between structure and function for these humoral mediators of inflammation.

Amino Acid Sequence↗