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Histopathology of humorally mediated anti-glomerular basement membrane (GBM) glomerulonephritis in mice


Le Hir, M (2004). Histopathology of humorally mediated anti-glomerular basement membrane (GBM) glomerulonephritis in mice. Nephrology, Dialysis, Transplantation, 19(7):1875-1880.

Abstract

Background. From a diagnostic point of view it would be important to learn more about the relationship between the immune responses underlying glomerulonephritis and the patterns of glomerular lesions. A murine model of anti-GBM glomerulonephritis in which inflammation is driven by delayed-type hypersensitivity (DTH) has been studied extensively. The aim of this study was to uncover histological features that might be specific for anti-GBM glomerulonephritis driven by a humoral immune response. Methods. BALB/c mice were immunized with rabbit IgG in incomplete Freund's adjuvant. Six days later, on day 0, they received rabbit anti-GBM serum intravenously. Proteinuria was assessed with dipsticks. Mice were killed on days 4, 8 or 14. Kidneys from days 4 and 8 were processed for immunofluorescence and histology. On day 14 mice were perfusion-fixed for electron microscopy. Results. Proteinuria started on day 3. Autologous IgG and of C3 were found along the GBM. There was only slight infiltration with macrophages and no measurable infiltration by CD4 T cells, indicating the virtual absence of DTH. Besides infiltration with neutrophils there were little histological alterations on day 4. On day 8 many loops were hyalinized. On day 14, cellular crescents were found in 23% of glomeruli. Subendothelial spaces contained hyaline material, cells and fibrin. Podocytes displayed effacement of foot processes and apical microprotrusions. Podocyte bridges were common. These alterations were identical to those reported in the standard model that produces a DTH-like inflammation. Conclusion. The qualitative pattern of histological damage in a murine model of anti-GBM glomerulonephritis does not depend on the underlying immunological process

Abstract

Background. From a diagnostic point of view it would be important to learn more about the relationship between the immune responses underlying glomerulonephritis and the patterns of glomerular lesions. A murine model of anti-GBM glomerulonephritis in which inflammation is driven by delayed-type hypersensitivity (DTH) has been studied extensively. The aim of this study was to uncover histological features that might be specific for anti-GBM glomerulonephritis driven by a humoral immune response. Methods. BALB/c mice were immunized with rabbit IgG in incomplete Freund's adjuvant. Six days later, on day 0, they received rabbit anti-GBM serum intravenously. Proteinuria was assessed with dipsticks. Mice were killed on days 4, 8 or 14. Kidneys from days 4 and 8 were processed for immunofluorescence and histology. On day 14 mice were perfusion-fixed for electron microscopy. Results. Proteinuria started on day 3. Autologous IgG and of C3 were found along the GBM. There was only slight infiltration with macrophages and no measurable infiltration by CD4 T cells, indicating the virtual absence of DTH. Besides infiltration with neutrophils there were little histological alterations on day 4. On day 8 many loops were hyalinized. On day 14, cellular crescents were found in 23% of glomeruli. Subendothelial spaces contained hyaline material, cells and fibrin. Podocytes displayed effacement of foot processes and apical microprotrusions. Podocyte bridges were common. These alterations were identical to those reported in the standard model that produces a DTH-like inflammation. Conclusion. The qualitative pattern of histological damage in a murine model of anti-GBM glomerulonephritis does not depend on the underlying immunological process

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Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Health Sciences > Nephrology
Health Sciences > Transplantation
Language:English
Date:1 July 2004
Deposited On:18 Oct 2018 15:48
Last Modified:09 Apr 2020 00:09
Publisher:Oxford University Press
ISSN:0931-0509
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/ndt/gfh281
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101093ndtgfh281 (Library Catalogue)
PubMed ID:15128887

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