Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using highly cationic polyethleneimine, alteration of glomerular anionic sites were evaluated ultrastructurally in two types of rat glomerulonephritis (GN); chronic serum sickness GN and heterologous (passive) or autologous (active) Heymann's GN. Daily i.v. injections of egg white lysozyme in physiologic saline into presensitized rats led to the formation of numerous mesangial and subepithelial deposits. In the non-proteinuric period in which immune deposits were localized predominantly in the mesangium, anionic sites of the laminae rarae and the epithelial cell coat were clearly observed. In the subsequent proteinuric period in which numerous subepithelial deposits were superimposed, a broad loss of anionic sites in the epithelial cell coat was seen. Splitting and focal loss of anionic sites on the lamina rara externa adjacent to the subepithelial deposits were commonly observed both in passive and active Heymann's GN and in lysozyme GN. These findings indicate that the subepithelial deposits are closely involved in the development of proteinuria by injuring the anionic sites, especially those on lamina rare externa of the glomerular basement membrane.
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PMID:Alteration of glomerular anionic sites by the development of subepithelial deposits in experimental glomerulonephritis in the rat. 613 11

The possibility of preservation and restoration of antigenicity of some antigens in paraffin-embedded tissue was evaluated by direct immunofluorescent technique on deparaffinized sections. Fixation with 96% ethanol-1% acetic acid, 10% neutral buffered formalin and p-formaldehyde was useful for the preservation of tissue antigens and immune deposits, whose antigenicity could be easily restored by trypsin digestion. Neutral buffered formalin was also a satisfactory fixative in immunofluorescent staining on lymphocyte/plasma cell-bound immunoglobulins. Fixation with alcohol-Bouin's fluid showed contrast results; feasible for staining of cell-bound immunoglobulins, but poor for that of glomerular immune deposits. After papain digestion, BSA and lysozyme, antigens of immune complexes, were easily detected in experimental chronic serum sickness glomerulonephritis. Pepsin was more efficient than trypsin in restoring the antigenicity of renal tissue antigens such as fibronectin and polyantigenic basement membrane, but the brush border antigen of the proximal renal tubules was frail to the pepsin digestion. In general, the enzymatic digestion time necessary for the restoration of antigenicity was in parallel with fixation time. Results obtained have shown that deparaffinized sections could be used as satisfactory substrate for immunohistochemistry when proper fixation and efficient proteolytic enzymatic pretreatments were performed.
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PMID:Restoration of antigenicity of tissue antigens, cell-bound immunoglobulins and immune deposits in paraffin-embedded tissue. The influence of fixation and proteolytic enzymatic digestion. 643 48

Epimembranous glomerular deposition of circulating immune complexes in considered to be the pathogenesis of immune complex glomerulonephritis, based on experiments in serum sickness glomerulopathy. A subepithelial localization of immune aggregates, however, was never obtained after the intravenous injection of preformed immune complexes. Recent studies on heterologous immune complex glomerulonephritis provide evidence of in situ formation of subepithelial glomerular immune complex aggregates as a second pathogenetic mechanism. We investigated the existence of a comparable mechanism in a serum sickness model of glomerulonephritis. A passive immune complex glomerulopathy involving lysozyme/antilysozyme and bovine serum albumin (BSA)/anti-BSA was used to investigate this thesis. Alternating perfusion of a kidney with antigen and antibody resulted in a granular deposition of both components along the glomerular basement membrane (GBM). The deposits of immune aggregates were localized exclusively along the epithelial side of the GBM and were still present 3 days after the perfusion. Control perfusions with preformed immune complexes or with either BSA or anti-BSA alone did not result in subepithelial deposition. Conclusion. The alternating excess of antigen and antibody in the circulation might result in in situ formation of immune complexes localized at the epithelial side of the GBM.
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PMID:In situ formation of subepithelial glomerular immune complexes in passive serum sickness. 644 23

The evolution of proteinuria in rabbits with experimentally induced chronic serum sickness was followed up longitudinally by analytical and quantitative assays. The results suggest that sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) is a more sensitive index of kidney malfunction than are total-protein assays or the quantitation of albumin and lysozyme. In some rabbits that showed abnormal proteinuria by SDS-PAGE, no histologic evidence of pathologic damage or of deposition of immune complexes in the kidneys was found. This suggests that SDS-PAGE may detect functional alterations at early stages of kidney damage when the lesions are either undetectable or reversible. In one rabbit that was killed after normalization of the proteinuria, immunofluorescence tests indicated deposition of C3, IgG, and fibrinogen, but there was no histologic evidence of kidney damage.
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PMID:Experimental model of chronic serum sickness. Relationships between proteinuria, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and glomerular and extraglomerular renal pathology. 699 Aug 90