Expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in an animal model of renal interstitial fibrosis induced by unilateral ureteral obstruction

Citation
J. Kriegsmann et al., Expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in an animal model of renal interstitial fibrosis induced by unilateral ureteral obstruction, EXP TOX PAT, 52(3), 2000, pp. 185-191
Citations number
36
Categorie Soggetti
Pharmacology & Toxicology
Journal title
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
ISSN journal
09402993 → ACNP
Volume
52
Issue
3
Year of publication
2000
Pages
185 - 191
Database
ISI
SICI code
0940-2993(200006)52:3<185:EOL(AI>2.0.ZU;2-A
Abstract
Unilateral ureteral obstruction (UUO) has been used as an experimental mode l to induce tubulointerstitial damage and interstitial fibrosis. UUO is cha racterized by cellular proliferation, accumulation of inflammatory cells, a nd subsequent replacement of renal parenchyma by fibrous tissue. The influx of inflammatory cells into the renal interstitium is mediated by adhesion molecules. In this study, the development of fibrosis in the UUO model of t he rat was examined and its relation to the time course of LFA-1 and ICAM-1 expression was assessed by immunohistochemistry. An increase in interstiti al connective tissue was detected on day 10 after UUO, with a maximum on da y 35. After unilateral ureteral obstruction, LFA-I was prominently expresse d in interstitial infiltrates, and to a lesser degree in glomerular areas. An initial increase in LFA-1-positive cells was noted already on day 10, wi th a maximum on day 20 and a decline on day 25. During the time course of 3 5 days after UUO, we observed an increase in ICAM-1 expression in the vascu lar endothelium, in tubular epithelium and in interstitial areas. This stud y shows that LFA-I expression and ICAM-1 expression are concordant and that this process is associated with increasing interstitial fibrosis. ICAM-1 i nterstitial tissue may facilitate the homing and persistence of an intersti tial infiltrate by ICAM-1/LFA-1 interactions, thereby preceding the develop ment of renal interstitial fibrosis.