Initiation and evolution of interstitial leukocytic infiltration in experimental glomerulonephritis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1991-09

AUTHORS

H Y Lan, D J Paterson, R C Atkins

ABSTRACT

Most forms of glomerulonephritis have a significant interstitial leukocytic infiltrate which is associated with disease progression. However, there is little data concerning the timing, initial location, and development of this interstitial component. Therefore, we have addressed these issues in a study of passive accelerated anti-GBM glomerulonephritis in the rat. In this model, interstitial leukocytic infiltration was an early event in the disease process with a significant infiltrate apparent at 12 hours after administration of nephrotoxic serum (NTS). This initial infiltrate was restricted to a perivascular sheath surrounding the hilar arterioles. The sheath infiltrate then spread to include the whole hilar area by day 1, the entire periglomerular area by day 3, and became widespread throughout the cortical tubulointerstitium by day 7. The early sheath infiltrate was composed of macrophages and T cells. Both cell types continued to increase as the infiltrate expanded, and a significant accumulation of activated cells (IL-2R+) was evident from day 7 onwards. There was a highly significant correlation between interstitial macrophage infiltration and renal function impairment, proteinuria, and histologic damage. Interstitial T cell infiltration correlated with proteinuria and histologic damage, while the appearance of immune-activated mononuclear cells (IL-2R+) exhibited a highly significant correlation with all disease parameters. This study demonstrates the importance of the glomerular hilar arteriolar region as a focus for mononuclear leucocytic migration and accumulation which not only affects the structure and function of the glomerulus but subsequently the entire tubulointerstitium. More... »

PAGES

425-433

References to SciGraph publications

  • 1985. The Heterogeneity of Mononuclear Phagocytes in Lymphoid Organs: Distinct Macrophage Subpopulations in Rat Recognized by Monoclonal Antibodies ED1, ED2 and ED3 in MICROENVIRONMENTS IN THE LYMPHOID SYSTEM
  • 1990-04. Contribution of mononuclear leucocytes to the progression of experimental focal glomerular sclerosis in KIDNEY INTERNATIONAL
  • 1987-04. Leukocyte analysis using monoclonal antibodies in human glomerulonephritis in KIDNEY INTERNATIONAL
  • 1989-12. Expression of leucocyte and lymphocyte adhesion molecules in the human kidney in KIDNEY INTERNATIONAL
  • 1989. Adhesion Receptors Regulate Antigen-Specific Interactions, Localization, and Differentiation in the Immune System in PROGRESS IN IMMUNOLOGY
  • 1985-03. T lymphocyte participation in antibody-induced experimental glomerulonephritis in KIDNEY INTERNATIONAL
  • 1989. Cytokine Induced Changes in the Endothelial Cell Surface Membrane: Significance for Lymphocyte Traffic in Inflammation in PROGRESS IN IMMUNOLOGY
  • 1990-01. Lupus nephritis: Correlation of interstitial cells with glomerular function in KIDNEY INTERNATIONAL
  • 1991. Pathogenesis of Glomerulonephritis — 1990 in NEPHROLOGY
  • 1982-09. Macrophages and cellular immunity in experimental glomerulonephritis in SEMINARS IN IMMUNOPATHOLOGY
  • 1982-09. Cellular immune mechanisms in human glomerulonephritis: The role of mononuclear leucocytes in SEMINARS IN IMMUNOPATHOLOGY
  • 1989-07. Paracrine and autocrine functions of glomerular mesangial cells in JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ki.1991.229

    DOI

    http://dx.doi.org/10.1038/ki.1991.229

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1026459133

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/1787643


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    52 schema:description Most forms of glomerulonephritis have a significant interstitial leukocytic infiltrate which is associated with disease progression. However, there is little data concerning the timing, initial location, and development of this interstitial component. Therefore, we have addressed these issues in a study of passive accelerated anti-GBM glomerulonephritis in the rat. In this model, interstitial leukocytic infiltration was an early event in the disease process with a significant infiltrate apparent at 12 hours after administration of nephrotoxic serum (NTS). This initial infiltrate was restricted to a perivascular sheath surrounding the hilar arterioles. The sheath infiltrate then spread to include the whole hilar area by day 1, the entire periglomerular area by day 3, and became widespread throughout the cortical tubulointerstitium by day 7. The early sheath infiltrate was composed of macrophages and T cells. Both cell types continued to increase as the infiltrate expanded, and a significant accumulation of activated cells (IL-2R+) was evident from day 7 onwards. There was a highly significant correlation between interstitial macrophage infiltration and renal function impairment, proteinuria, and histologic damage. Interstitial T cell infiltration correlated with proteinuria and histologic damage, while the appearance of immune-activated mononuclear cells (IL-2R+) exhibited a highly significant correlation with all disease parameters. This study demonstrates the importance of the glomerular hilar arteriolar region as a focus for mononuclear leucocytic migration and accumulation which not only affects the structure and function of the glomerulus but subsequently the entire tubulointerstitium.
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