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PubMed1981

Circulating immune complexes in bacillary and amebic dysentery.

In order to study the relationship between the presence of circulating immune complexes (CIC) and the severity and duration of acute dysentery, we studied 11 adults and 45 children in Bangladesh with bacillary and amebic dysentery, using the Raji cell and solid-phase C1q (C1q-SPA) assays. CIC were found in 70% of patients with shigellosis and in all eight cases of amebic dysentery. Mild shigellosis was associated with positive samples in the first week of clinical illness, whereas severe cases, including those with the hemolytic-uremic syndrome, had negative admission assays but positive convalescent assays. Samples positive in the first two weeks of illness were more likely positive by the Raji cell assay alone whereas samples in the third and fourth weeks of illness were positive more often by the C1q-SPA assay. Only one shigellosis sample was positive by both assays. In amebiasis 11 of 13 samples were positive by the Raji assay alone. In dysenteric disease circulating immune complexes probably represents the failure of the inflamed mucosa to exclude microbial and dietary antigens, and suggests that the presence of CIC in any intestinal disease must be interpreted with caution.

Anemia, Hemolytic↗

PubMed2003

Immune complex-associated thrombocytopenic purpura syndrome in sexually mature Göttingen minipigs.

Eleven cases of thrombocytopenic purpura (TP) in sexually mature male or female Göttingen minipigs occurred sporadically over 3 1/2 years in a closed breeding colony protected by strict barrier conditions. Typical clinical signs of TP, including extensive subcutaneous haemorrhages, were seen in all affected animals. Haematological abnormalities included marked thrombocytopenia and anaemia. A consistent histopathological finding was the presence of membranoproliferative lesions in the renal glomeruli. Immunohistochemically, glomerular deposits were positively labelled for complement factor C1q and often also for immunoglobulins. Bone marrow findings consisting of increased numbers of immature and apoptotic megakaryocytes were compatible with a state of increased platelet consumption. Based on the combined presence of thrombocytopenia and renal immune complexes, it is suggested that the syndrome was related to a type III hypersensitivity reaction. However, further studies are needed to verify this hypothesis.

Anemia↗

PubMed1984

[Is the demonstration of immune complex useful in the activity assessment of chronic polyarthritis?].

In a prospective and controlled long-term study of 39 patients suffering from rheumatoid arthritis (RA), various blood parameters including the C1q-binding test (fluid phase) and the Rajicell test were performed. Blood samples were taken every three months during an observation period of eighteen months and compared with disease activity. According to these sequential analyses, immune complexes determined in the serum by these two tests do not always reflect disease activity expressed by addition of active joints. These results confirmed that the C1q-binding test often closely reflects disease activity. In patients with RA and extraarticular manifestations the C1q-binding test continuously showed increased concentrations of circulating immune complexes in the serum. In patients with predominant vasculitis the regular determination of circulating immune complexes is the best means of showing disease activity. This latter observation is especially true in patients with malignant RA. On the whole, the clinical significance of regularly performed assay for detection of immune complexes in RA appears questionable.

Adult↗

PubMed1989

Histopathological and immunofluorescence study of the choroid plexus in hepatosplenic schistosomiasis mansoni.

A histopathological and immunofluorescence (IMF) study of the choroid plexus was performed in 8 cases of hepatosplenic schistosomiasis mansoni and in 20 cases which had resulted in death with no evidence of liver or brain involvement by schistosomiasis or other disease process, and in which renal disease and arterial hypertension were also excluded (control group). IgA, IgG, IgM, C3, and C1q were investigated. Positive IMF in the choroid plexus was found in 75% of the schistosomiasis group. IgA and IgG were the immunoglobulins (Ig) most frequently found. C3 was also commonplace. Histologic examination of the choroid plexus showed changes in 87.5% of the schistosomiasis group. The most frequently found change was characterized by focal, linear, occasionally nodular, subepithelial deposition of a homogeneous, acidophilic, and PAS positive substance, apparently in relation to the epithelial basement membrane, with thickening of this structure. In the control group, the IMF in the choroid plexus was negative in all cases, and only 2 cases (10%) presented histopathological changes of the choroid plexus with a pattern similar to that of the schistosomiasis group. The demonstration of the deposition of Ig and fractions of the complement system, and of histological changes in the choroid plexus in a liver disease which is known to exhibit circulating immune complexes and glomerulopathy with deposition of Ig and fractions of the complement system suggests an etiopathogenetic relationship between both findings.

Adolescent↗

PubMed1991

Surfactant protein A is opsonin in phagocytosis of herpes simplex virus type 1 by rat alveolar macrophages.

In the present study we used flow cytometry to investigate the phagocytosis of fluorescein isothiocyanate-labeled herpes simplex virus type 1 (FITC-HSV-1) by rat alveolar macrophages and the effects of surfactant protein A (SP-A) on this process. The phagocytosis of FITC-HSV-1 by alveolar macrophages, which was studied as a model for virus phagocytosis in general, was strongly enhanced in the presence of SP-A. The SP-A-mediated phagocytosis was time and concentration dependent, reaching a maximal level after 15 min of incubation and at an SP-A concentration of 5 micrograms/ml. Using a fluorescence quenching technique, we could show that at least 65% of the viruses were indeed internalized by the macrophages. The addition of SP-A to the system was sufficient for the phagocytosis of FITC-HSV-1 by the alveolar macrophages, suggesting that SP-A acts as an opsonin. This hypothesis was further strengthened by the observation that F(ab')2 fragments of immunoglobulin G directed against SP-A could abolish FITC-HSV-1 phagocytosis by alveolar macrophages preincubated with SP-A. Comparing the opsonic capacity of serum and SP-A, SP-A proved to be twice as potent as serum in stimulating phagocytosis of FITC-HSV-1 by alveolar macrophages. Complement factor C1q, which is known to possess a similar collagen-like domain as SP-A, did not stimulate phagocytosis of FITC-HSV-1 by alveolar macrophages nor did it inhibit SP-A-mediated HSV-1 phagocytosis. This study demonstrates that SP-A may play an important role in the antiviral defenses of the lung.

Animals↗

PubMed1982

Nonsystemic mesangiopathic glomerulonephritis with "full house" immunofluorescence. Pathological and clinical observation in five patients.

Five patients, four women and one man, between the ages of 19-38 years developed nonsystemic renal glomerular disease. All presented with proteinuria (two with the nephrotic syndrome) and four had microhematuria. Biopsy revealed mesangial and focal proliferative glomerulonephritis with "full house" immunofluorescence (deposits containing IgG, IgM, IgA, C1q, C4, C3). The deposits were located primarily in the mesangium. After 10-58 months of follow-up, none has demonstrated any evidence of systemic illness. All had persistent proteinuria and two have shown evidence of progression of disease but none was in established renal failure. Because of the "full house" immunofluorescence, this entity resembles mesangial lupus nephritis and may be the nonsystemic counterpart of the latter illness analogous to the proposed relationship of IgA nephropathy to Henoch-Schönlein nephritis.

Adult↗

PubMed1997

Phagocytosis of viable Candida albicans by alveolar macrophages: lack of opsonin function of surfactant protein A.

Surfactant protein A (SP-A) contributes to host defense by opsonizing microbial organisms for phagocytosis by alveolar macrophages (AM). The role of SP-A as opsonin for phagocytosis of Candida albicans was analyzed. AM in suspension exhibited no phagocytosis of nonopsonized yeast. This was not increased by SP-A, whether provided for preincubation of AM or yeast or present during coincubation. However, the engulfment of serum-opsonized yeast by AM in suspension was inhibited by SP-A. This inhibitory effect was mimicked by complement subcomponent C1q and concanavalin A but not by type IV collagen. SP-A did not interfere with phagocytosis of serum-opsonized yeast by adherent AM, monocytes, neutrophils, or peritoneal macrophages. SP-A lacks function as an opsonin for the phagocytosis of C. albicans by AM but interferes with binding of yeast to AM, inhibiting subsequent ingestion. The role of SP-A as an alveolar space opsonin may thus critically depend on the microbial species involved.

Animals↗

PubMed1981

The detection of circulating immune complexes in normal subjects using four different methods.

336 estimations of circulating immune complexes have been performed on the sera of blood donors by four different methods: the solid phase C1q binding test, the fluid phase C1q binding assay, the conglutinin binding test and the Raji cell radio-immune assay. Between 68 and 105 subjects were used in the analysis of each method. With the first three methods, immune complex levels showed a peaked asymmetric distribution with a positive tail including about 10% of subjects, whereas using the fourth method immune complex values were widely spread. No difference in immune complex values between males and females was found. There was a significant trend for the prevalence of immune complexes to increase with age when methods were used which detect complexes through C3 binding. In a further 13 subjects tested at regular intervals during a period of 24 hours, using the fluid phase C1q binding test, significant variations in immune complex levels were found but no consistent pattern of variation at different hours of the day or after meals could be seen. In studies of immune complexes on small groups of patients it is advisable to test multiple samples from te same subjects taken at different times, whereas when large series of patients are being studied results should be compared to those obtained with age matched controls.

Adult↗

PubMed2001

Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro.

We have previously developed and characterized isolated microglia and astrocyte cultures from rapid (<4 h) brain autopsies of Alzheimer's disease (AD) and nondemented elderly control (ND) patients. In the present study, we evaluate the inflammatory repertoire of AD and ND microglia cultured from white matter (corpus callosum) and gray matter (superior frontal gyrus) with respect to three major proinflammatory cytokines, three chemokines, a classical pathway complement component, a scavenger cell growth factor, and a reactive nitrogen intermediate. Significant, dose-dependent increases in the production of pro-interleukin-1beta (pro-IL-1beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory peptide-1alpha (MIP-1alpha), IL-8, and macrophage colony-stimulating factor (M-CSF) were observed after exposure to pre-aggregated amyloid beta peptide (1-42) (Abeta1-42). Across constitutive and Abeta-stimulated conditions, secretion of complement component C1q, a reactive nitrogen intermediate, and M-CSF was significantly higher in AD compared with ND microglia. Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators.

Aged↗

PubMed1999

Surfactant protein A down-regulates proinflammatory cytokine production evoked by Candida albicans in human alveolar macrophages and monocytes.

Surfactant protein A (SP-A) has been implicated in the regulation of pulmonary host defense and inflammatory events. We analyzed the impact of SP-A on the Candida albicans-induced cytokine response in human alveolar macrophages (AM) and its precursor cells, the monocytes, which rapidly expand the alveolar mononuclear phagocyte pool under inflammatory conditions. Both recombinant human SP-A and natural canine SP-A were employed. SP-A dose-dependently down-regulated the proinflammatory cytokine response of AM and monocytes to both viable and nonviable Candida, including TNF-alpha, IL-1beta, macrophage inflammatory protein-1alpha, and monocyte chemoattractant protein-1. In contrast, SP-A did not affect the baseline liberation of these cytokines. The release of the antiinflammatory cytokines IL-1 receptor antagonist and IL-6 was not inhibited by SP-A under baseline conditions and in response to fungal challenge. The inhibitory effect of SP-A on proinflammatory cytokine release was retained upon reassembly of the apoprotein with natural surfactant lipids and in the presence of serum constituents, for mimicry of plasma leakage into the alveolar space. It was not reproduced by the homologous proteins complement component C1q and type IV collagen. It was independent of Candida-SP-A binding and phagocyte C1q receptor occupancy, but apparently demanded SP-A internalization by the mononuclear phagocytes, effecting down-regulation of proinflammatory cytokine synthesis at the transcriptional level. We conclude that SP-A limits excessive proinflammatory cytokine release in AM and monocytes confronted with fungal challenge in the alveolar compartment. These data lend further credit to an important physiological role of SP-A in regulating alveolar host defense and inflammation.

Blood Proteins↗

PubMed1995

Improved method for measuring C1-r-C1-s-(C1 inh)2 complexes by an enzyme-linked immunosorbent assay.

Measurement of C1-r-C1-s-(C1 inh)2 complexes in serum or plasma by enzyme-linked immunosorbent assay (ELISA) has been proposed as a relatively convenient and sensitive means for assessing C1 activation. However, interference by unactivated C1q (r-s)2 at low serum or plasma dilutions has resulted in estimates that vary widely with the degree of serum or plasma dilution. Precipitating the interfering C1q (r-s)2 with 6% polyethylene glycol has been proposed to resolve this problem, but here it is shown that this procedure also precipitates or coprecipitates some of the C1-r-C1-s-(C1 inh)2 complexes. Satisfactory results have been achieved without PEG precipitation by testing high plasma dilutions under conditions where there is a sufficient excess of anti-C1s coating the microtitration plate wells that removal of C1q (r-s)2 is not necessary. Optimizing conditions for quantitating these complexes at high dilution have been investigated. The mean normal EDTA plasma C1-r-C1-s-(C1 inh)2 complex measurement was 36.6 +/- 7.0 (S.D.) ELISA units with a 95% confidence interval of 19.5-47.6u. Besides providing a sensitive assay for C1 activation, measuring C1-r-C1-s-(C1 inh)2 complexes may help to clarify the pathophysiologic mechanisms resulting from C1 inh deficiency under various conditions.

Adult↗

PubMed1985

[Characterization of immune complexes in normal pregnancies].

There are many reports on the immune complexes in normal pregnancies. Nevertheless, even the presence of immune complexes in normal pregnancies have not been clarified, and the immune complexes have not been clearly characterized. So, in this report, I try to make clear whether immune complexes are present in normal pregnancies or not, and then to analyze the immune complexes in normal pregnancies. The results are as follows: The immune complex (IC) levels measured by the C1q binding test rose in first trimester, and dropped to the normal range in the second and third trimesters. The IgG-IC levels increased in the first trimester and decreased to the normal range in the second and third trimesters, but the IgM-IC levels were not changed during normal pregnancies in the solid phase anti C3 radioimmunoassay. The ICs in normal pregnancies were analyzed using gel filtration. IgG-ICs were detected in the first trimester and the third trimester of normal pregnancies, and the molecular weights were about 290,000. IgG-ICs were separated from another immunoglobulin class IC using a DEAE-affigel blue column. ICs in normal pregnancies were mainly IgG-IC and there were only a few IgM-ICs in normal pregnancies. IgG-ICs were present in normal pregnancies, but neither the classical pathway nor the alternative pathway of the complement system was found to be activated by the two-dimensional electroimmunodiffusion method using anti C3 and C1s. So, IgG-IC in normal pregnancies did not seem to be pathological.

Antigen-Antibody Complex↗

PubMed1996

The A-domain of integrin alpha 2 binds specifically to a range of collagens but is not a general receptor for the collagenous motif.

Integrin alpha 2 beta 1 is a major cellular receptor for collagens, but the molecular basis of its function is unknown. The alpha 2 subunit contains a von Willebrand factor A-domain (I-domain) in its N-terminal region, and it has been demonstrated recently that this domain binds specifically to collagen I. This interaction requires divalent cations (e.g., Mg2+) and native collagen conformation, as does binding of the parent integrin to collagen. The alpha 2 A-domain therefore has a number of functional similarities to the parent integrin, alpha 2 beta 1. However, while sequence specificity has been demonstrated for the parent integrin, no such observations have been made for the A-domain. In particular, it is not known whether the A-domain is responsible for sequence-specific recognition of collagens or whether it binds to the genetic collagenous motif. To investigate the ligand specificity of the alpha 2 A-domain, its binding to a range of collagenous ligands has been studied, with cation dependence, collagen triple-helicity, and inhibition by function-blocking antibodies as criteria for specificity. Binding of the parent integrin was examined for comparison. The alpha 2 A-domain was found to bind specifically to collagens I, II, IV and XI. The complement component C1q has a collagenous domain but this was unable to support specific binding of alpha 2 A-domain or alpha 2 beta 1. Furthermore, synthetic triple-helical collagenous peptides failed to act as specific ligands. In conclusion, the alpha 2 A-domain binds specifically to a range of extracellular matrix collagens, but it is not a receptor for all collagenous triple helices. By inference, these findings indicate the existence of an integrin-specific sequence motif within collagenous ligands recognised by the alpha 2 A-domain.

Antigens, CD↗

PubMed1991

Nonamyloidotic fibrillary glomerulopathy. Report of a case and review of the literature.

A 29-year-old man had oedema, proteinuria in nephrotic range, haematuria and cardiac arrhythmia (second grade atrioventricular block). The pathologic findings of kidney biopsy showed in light microscopy diffuse mesangial matrix increase with mild mesangial proliferation and variable thickening of the glomerular capillary walls. IgG, c3 and c1q were intensely fluorescent and exhibited a diffuse granular pattern in mesangial areas and along the capillary walls. Both kappa and lambda chains were weakly positive in the same pattern. Ultrastructurally, microfibrils of about 20 nm in width were seen to be deposited in mesangial areas and along the glomerular basement membranes. Congo red stain and metachromasia were negative. Neither cryoglobulinaemia nor paraproteinaemia including light chains were found. The aetiology of nonamyloidotic fibrillary glomerulopathy is unknown and no clear-cut clinical or pathologic pattern has emerged. It may represent more than one disease process with a common morphologic expression.

Adult↗

PubMed1981

The effect of a protein meal on three fluid-phase assays for circulating immune complexes.

Serial blood samples were taken from eight patients with systemic lupus erythematosus and five normal controls before and after a standard meal containing 20 g of protein. The samples were assayed for circulating immune complexes by the fluid-phase C1q, monoclonal rheumatoid factor and conglutinin-binding assays. No significant differences were seen in the post- as compared to the pre-prandial levels of circulating immune complexes. In neither controls nor patients did circulating complexes appear for the first time within 90 min after starting the meal. We conclude that if systemic antigen--antibody reactions occur soon after a protein meal they are not detected by the polyethylene glycol-dependent tests in current use and do not appear to influence the immediate clearance of endogenous immune complexes.

Antigen-Antibody Complex↗

PubMed1984

Correlation of C3d fixing circulating immune complexes with disease activity and clinical parameters in patients with systemic lupus erythematosus.

Using anti-C3d as a solid phase reagent, C3d fixing circulating immune complexes (CIC) were detected in sera from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis, membranous nephropathy and IgA nephropathy. Particularly, sera from SLE showed the highest CIC levels and highest incidence of positivity among these diseases. In the 51 serum samples from 48 patients with SLE we studied, the CIC detected by the anti-C3d assay correlated well (P less than 0.01) with the CIC detected by the solid phase C1q assay, but not with those detected by the conglutinin assay. In addition, the CIC detected by the anti-C3d assay correlated more significantly (P less than 0.001) with disease activity, as well as some clinical parameters (serum anti-dsDNA antibodies, CH50 and C3 levels) than CIC detected by the other two assays of SLE sera. The anti-C3d binding materials were found to be of intermediate (8-19S) and small (7S) sizes in a small number of SLE sera which we analysed.

Antigen-Antibody Complex↗

PubMed1985

A rapid and reproducible method for the analysis of immune complexes using affinity chromatography and Western blotting.

A new procedure which couples different analytical techniques in a format permitting the rapid analysis of immune complex components is described. Complexes obtained from sera by polyethylene glycol (PEG) precipitation were resuspended and then added, using a batch method, to antibody coupled to Sepharose beads. Antibody directed against either human C1q or human C3c were used in the present study. Bound immune complexes were washed and then eluted from the Sepharose by sodium dodecyl sulphate (SDS) treatment and simultaneously reduced with dithiothreitol. Individual components were separated by SDS gradient polyacrylamide gel electrophoresis and then transferred to nitrocellulose by Western blotting. Individual strips of nitrocellulose were investigated using specific antisera and a radiolabelled probe. Immune complexes (IC) isolated from the sera of 7 rheumatoid arthritis (RA) patients were analysed using this method and the results obtained for both affinity adsorbents compared.

Antigen-Antibody Complex↗

PubMed1982

Nephrotic syndrome with diffuse mesangial IgM deposits.

The renal biopsies of three cases of nephrotic syndrome were examined by light, electron and immunofluorescent microscopy. The histological appearances were characterized by mild mesangial proliferation and extensive diffuse and global deposition of IgM in the mesangial areas, with some in the capillary walls. C3 and C1q were also identified in two of the cases. Electron microscopy revealed scanty electron dense deposits in the mesangial areas and subendothelial spaces. All three patients had a nephrotic proteinuria but no hematuria. None had hypertension or renal dysfunction throughout their clinical courses. They received steroid therapy and achieved complete remission within one month after the initial treatment. Two of them, however, have had frequent relapses whenever the dosage of steroid was gradually reduced. One case continues to be free of proteinuria. These cases indicate that a distinct disease may exist, because of the uniform immunofluorescent findings. We wish to designate it as IgM nephropathy.

Adult↗