Intercellular adhesion molecule 1 mediates mononuclear cell infiltration into rat glomeruli after renal ablation

Nephron. 1998;79(1):91-8. doi: 10.1159/000044997.


Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 +/- 0.15 vs. 0.61 +/- 0.13; p < 0.01) and 2 weeks (1.31 +/- 0.17 vs. 0.51 +/- 0.09; p < 0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 +/- 0.16 vs. 0.99 +/- 0.08; p < 0.01) and 2 weeks (3.14 +/- 0.14 vs. 0.89 +/- 0.07; p < 0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 +/- 0.19) and 2 weeks (1.46 +/- 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomeruli following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology
  • Antigens, CD / immunology
  • Disease Models, Animal
  • Gene Expression Regulation / genetics
  • Immunohistochemistry
  • Intercellular Adhesion Molecule-1 / physiology*
  • Kidney Glomerulus / physiopathology*
  • Leukocytes, Mononuclear / metabolism*
  • Macrophages / metabolism
  • Male
  • Nephrectomy / adverse effects*
  • Rats
  • Rats, Sprague-Dawley


  • Antibodies, Monoclonal
  • Antigens, CD
  • Intercellular Adhesion Molecule-1