Evidence for the involvement of IgE-basophil system in acute serum sickness.
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The role of the basophils in acute serum sickness of rabbits was examined by monitoring daily the absolute number of basophils before, during and after the disease period. After antigen (bovine serum albumin, BSA) elimination, levels of serum IgE and in vitro basophil degranulation in the presence of BSA were determined. The results showed that the onset of glomerular lesions depends upon the simultaneous occurrence of circulating immune complexes greater than 19 S and of an in vivo basophil depletion--probably equivalent to degranulation--reaching 70% of the pre-disease number. Post-disease antigen-dependent in vitro degranulation of the basophils and levels of serum IgE anti BSA did not prove to be good indexes of basophil sensitization. Our data suggest that basophils are instrumental at early stages of the deposition of immune complexes, most probably through their sensitization by membrane-bound IgE antibodies. (+info)
Cyclosporin A reduces expression of adhesion molecules in the kidney of rats with chronic serum sickness.
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Treatment with cyclosporin A (CsA) improves proteinuria and reduces renal cellular infiltration in chronic serum sickness (CSS). We examined if these effects were associated with a reduced renal expression of CD54 and its ligands, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and MHC class II molecules. We studied two groups of rats in which CSS was induced by daily injections of ovalbumin (OVA): a group treated with CsA (OVA.CsA group, n = 11) and a group that received no treatment (OVA.CSS group, n = 11). An additional group of five rats (control group) received only phosphate buffer. Immunostaining techniques were used to follow CSS and to study the expression of CD54, CD18, CD11b/c, IFN-gamma, TNF-alpha and MHC class molecules. Proteinuria (mg/24 h) was reduced from 248.2 +/- 73.1 (OVA.CCS group) to 14.5 +/- 13.1 with CsA treatment (P < 0.0001). The renal expression of CD54 and its ligands (CD18 and CD11b/c) was reduced by 50% to 75%. Correspondingly, there was a 60% to 85% reduction in the number of infiltrating leucocytes. The number of cells expressing TNF-alpha, IFN-gamma and MHC II molecules was also reduced. CsA reduces expression of CD54 and its ligands. This effect is associated with a reduction of cellular infiltration, IFN-gamma, TNF-alpha-producing cells and with MHC II expression in the kidney. These findings suggest that expression of adhesion molecules plays a critical role in CSS and underline the importance of cellular immunity in this experimental model. (+info)
Demonstration of immunoglobulin containing deposits in glomerular basement membrane in experimental chronic serum sickness using horseradish peroxidase labelled antiserum.
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Horseradish peroxidase (HRP) labelled antibodies were used in rabbit glomerulonephritis to obtain localization of immunoglobulins in the glomerulus at a light and electron microscope level. Better localization of deposits was obtained with peroxidase labelled antiserum than with immunofluorescence at the light microscope level. Ultrastructurally, immunoglobulin localization was seen to correspond to the electron dense deposits demonstrated in and on the glomerular basement membrane by conventional microscopy. (+info)
Immunohistochemical analysis of human serum sickness glomerulonephritis.
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AIM: To analyze pathological and immunohistochemical characteristics of glomerulonephritis in human serum sickness. METHODS: Renal biopsy specimens from two female patients with serum sickness that ensued after application of anti-lymphocyte horse globulin for aplastic anemia were analyzed by light microscopy, immunofluorescence, and electron microscopy. To prove the depositions of foreign protein, frozen sections were incubated with fluorescein-conjugated anti-horse protein serum. Immunohistochemical analysis was performed on B5-fixed paraplast-embedded tissue or frozen acetone-fixed sections with the primary antibodies for molecules/cell markers CD35, CD43, CD45RO, CD68, CD2, lysozime, L26, and S100. RESULTS: Diffuse proliferating and necrotizing glomerulonephritis with crescents was found. There were coarse granular mesangial, subepithelial, subendothelial, and intramembranaceous deposits of mainly horse globulin, C3, and IgG. Most mesangium infiltrating cells were macrophages and T-lymphocytes. Electron microscopy revealed hypertrophy of podocytes, but immunohistochemistry did not show their normal CD35 (C3b-receptor) staining. Apart from epithelial cells, main crescent forming cells were macrophages and T-lymphocytes. Rare dendritic cells and abundant infiltration of macrophages, T-lymphocytes, and neutrophiles were found in the interstitium. CONCLUSION: In severe serum sickness, glomeruli and tubuli are destroyed beyond the range usually seen in other types of glomerulonephritis caused by immune complexes, except in cases with widespread crescents. Hypertrophy of podocytes and loss of their normal C3b-receptor staining has not yet been described in the literature. C3b-receptors on podocytes could play a role in pathogenesis of glomerular injury caused by immune complexes. (+info)
Passive serum sickness in the mouse: effect of interstrain differences on glomerular deposition of immune complexes.
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Glomerular uptake of passively administered immune complexes in mice differs in different inbred strains. The amount of immune material deposited in the glomeruli in the strains examined is inversely related to the susceptibility to immune complex induced anaphylaxis. The significance of these findings is discussed. (+info)
The effects of defibrination with ancrod in experimental allergic glomerular injury.
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Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events. (+info)
Detection of circulating soluble immune complexes in patients with various renal diseases.
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Sera from patients with various types of glomerulonephritis (GN) as well as sera from rabbits with acute serum sickness were studied for the presence of circulating immune complexes (IC). The method used is based on the observation that IC inhibit the uptake of IgG aggregates by guinea-pig peritoneal macrophages. Inhibition significantly greater than with normal human sera was found with sera of patients with membranous GN, membranoproliferative GN, focal glomerular sclerosis, minimal change nephrotic syndrome, acute septicaemic glomerular diseases and systemic lupus erythematous. IC were also detected in rabbits with acute serum sickness during the period of immune elimination. (+info)
Serum sickness-like reaction possibly associated with meropenem use.
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Serum sickness-like reactions most commonly occur secondary to drug administration. We describe a serum sickness-like reaction that was possibly associated with meropenem therapy. (+info)