VASCULAR ADHESION MOLECULE-1 AND INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION ON RAT-LIVER CELLS AFTER LIPOPOLYSACCHARIDE ADMINISTRATION IN-VIVO

During sepsis the infiltration of leukocytes plays a pivotal role in t issue damage. Induction of septic shock results in an early accumulati on of polymorphonuclear leukocytes in the liver (after 3 hours), which is followed by an infiltration of mononuclear phagocytes (after 30 ho urs). Expression of adhesion molecules may contribute to the migration of leukocytes to the site of inflammation. Therefore, in the present study we determined the expression of intercellular adhesion molecule- 1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) on hepatocytes, l iver endothelial cells, and Kupffer cells after lipopolysaccharide (LP S) treatment of rats in vivo. Parenchymal cells showed no constitutive expression of VCAM-1 and the expression could not be upregulated by L PS treatment in vivo, whereas Kupffer and endothelial cells had a low basal expression of VCAM-1 and this expression was increased 40-fold b y LPS treatment in vivo. All three cell types showed a basal expressio n if ICAM-1 and the expression on endothelial liver cells of untreated rats was two times higher than the expression on parenchymal and Kupf fer cells. Stimulation with LPS increased the expression if ICAM-12.5 times for parenchymal cells and approximately 4 times for endothelial and Kupper cells. It is concluded that the expression of adhesion mole cules may contribute to the influx of leukocytes during septic shock a nd, therefore, play a role in tissue damage during septic shock.