Nephrology Dialysis Transplantation, Vol 12, Issue 6 1122-1131, Copyright © 1997 by Oxford University Press
I Hauser, R Riess, B Hausknecht, H Thuringer and R Sterzel
Background. In vitro studies have
demonstrated that inflammatory mediators such as the cytokines TNF&agr;
and IL-1 upregulate or induce de novo expression of
cell adhesion molecules on endothelial and epithelial cells. In the present
study the expression of the cell adhesion molecules ICAM-1, VCAM-1,
E-selectin and PECAM-1 was investigated in renal biopsies from patients
with primary renal diseases (n=66) and from renal
allograft recipients (n=42).
Methods. Expression of the cell adhesion molecules was
determined by immunohistochemistry of frozen sections using monoclonal
antibodies directed against PECAM-1, ICAM-1, VCAM-1, E-selectin and MHC
class II molecules (APAAP method). Results and
Conclusions. PECAM-1 and ICAM-1 were expressed in the renal
vasculature and disappeared in obliterated glomeruli with endothelial cell
destruction. ICAM-1 but not PECAM-1 was upregulated in renal endothelia in
acute allograft rejection and inflammatory primary renal diseases. Tubular
de novo expression of ICAM-1 an dVCAM-1 correlated
with severe structural damage of the renal parenchyma including
interstitial fibrosis. Vascular and/or glomerular VCAM-1 and E-selectin
expression was pronounced in severe acute allograft rejection and also
reflected the intensity of inflammatory reactions in primary renal diseases
with or without autoimmune disorders. De novo
expression of VCAM-1 and E-selectin in renal vessels and/or glomeruli and
overexpression of ICAM-1 are markers of acute and severe inflammatory
processes in biopsies from allograft recipients and patients with primary
renal diseases. Keywords: E-selectin; ECAM-1;
inflammatory kidney disease; PECAM-1; transplantation; VCAM-1.
ORIGINAL ARTICLES
Expression of cell adhesion molecules in primary renal disease and renal allograft rejection
IV Medical Clinic, Department of Nephrology, University of Erlangen/Nurnberg, 90471 Nurnberg, Germany; Department of Pathology, City Hospital Nurnberg, Nurnberg, Germany; Corresponding author
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