Intrinsic renal cells are the major source of interleukin-1 beta synthesis in normal and diseased rat kidney

Nephrol Dial Transplant. 1997 Jun;12(6):1109-15. doi: 10.1093/ndt/12.6.1109.


Background: A number of studies have demonstrated a pathological role for interleukin-1 (IL-1) in experimental models of glomerulonephritis, but the cellular pattern of renal IL-1 production remains poorly characterized. The aim of this study, therefore, was to identify the cell types expressing IL-1 in normal and diseased rat kidney.

Methods: Renal IL-1 beta expression was examined in normal rats and during a 21-day time course of rat accelerated anti-GBM glomerulonephritis by northern blotting, in situ hybridization and double immunohistochemistry.

Results: Interleukin-1 beta mRNA expression was readily detectable in normal rat kidney by northern blot analysis and in situ hybridization. Immunohistochemistry staining demonstrated constitutive IL-1 beta expression by glomerular endothelial cells and cortical tubular epithelial cells. There was a marked increase in whole kidney IL-1 beta mRNA in rat anti-GBM glomerulonephritis. Glomerular IL-1 beta immunostaining was upregulated, being expressed by podocytes, mesangial cells and infiltrating macrophages, and was particularly prominent within glomerular crescents. Double staining with the ED1 antibody showed IL-1 beta expression in up to 13% of glomerular macrophages, whereas 48% of macrophages within crescents stained for IL-1 beta. However, the most marked increase in IL-1 beta expression was seen in cortical tubular epithelial cells, particularly in areas of tubular damage. In situ hybridization confirmed that tubular IL-1 beta staining was due to local cytokine synthesis rather than protein absorption.

Conclusions: This study has identified constitutive IL-1 beta expression by glomerular endothelium and tubular epithelial cells in normal rat kidney. In addition, the marked upregulation of IL-1 beta expression by intrinsic glomerular cells and tubules in rat anti-GBM disease suggests an important role for these cells in IL-1 dependent crescent formation and tubulointerstitial injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Endothelium / metabolism
  • Glomerulonephritis / metabolism*
  • Immunohistochemistry
  • In Situ Hybridization
  • Interleukin-1 / biosynthesis*
  • Interleukin-1 / genetics
  • Kidney / metabolism*
  • Kidney Glomerulus / immunology
  • Kidney Glomerulus / metabolism
  • Kidney Tubules / metabolism
  • Macrophages / metabolism
  • Male
  • RNA, Messenger / analysis
  • Rats
  • Rats, Sprague-Dawley


  • Interleukin-1
  • RNA, Messenger