title: Intercellular adhesion molecule 1 mediates mononuclear cell infiltration into rat glomeruli after renal ablation.
abstract: 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.
authors.affiliation: Department of Medicine III, Okayama University Medical School, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Miyatake
authors.forename: K
authors.initials: K
authors.lastname: Shikata
authors.forename: H
authors.initials: H
authors.lastname: Sugimoto
authors.forename: M
authors.initials: M
authors.lastname: Kushiro
authors.forename: Y
authors.initials: Y
authors.lastname: Shikata
authors.forename: S
authors.initials: S
authors.lastname: Ogawa
authors.forename: Y
authors.initials: Y
authors.lastname: Hayashi
authors.forename: M
authors.initials: M
authors.lastname: Miyasaka
authors.forename: H
authors.initials: H
authors.lastname: Makino
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D015703:Antigens, CD / Q000276:immunology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology*; D007678:Kidney Glomerulus / Q000503:physiopathology*; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D009392:Nephrectomy / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D018799:Intercellular Adhesion Molecule-1