Intercellular adhesion molecule-1 (ICAM-1) expression in the liver of patients with extrahepatic cholestasis.
ICAM-1 mediates the recruitment of neutrophils through the endothelium to the site of inflammation by the ICAM-1/Mac-1 and ICAM-1/LFA-1 adhesion pathways. In extrahepatic cholestasis, recruitment of neutrophils is a main feature of the inflammatory infiltrate in areas of parenchymal damage. The aim of the present study was to describe the light and electron microscopical localization of ICAM-1 expression in the liver of cholestatic patients. The peroxidase-antiperoxidase technique was used. Increased ICAM-1 expression was detected on sinusoidal endothelial and Kupffer cells. A de novo ICAM-1 expression was described on some Ito cells and the sinusoidal hepatocyte membrane in areas of parenchymal injury. In the portal areas of livers of cholestatic patients, ICAM-1 was observed on the endothelial surface of portal veins and on hepatic arteries. Occasionally, ICAM-1 was found on the surface of bile duct epithelia. It is suggested that ICAM-1 expression is up-regulated by cytokines like TNF-alpha, IL-1 and interferons released from activated Kupffer cells. The mechanisms of ICAM-1 upregulation and neutrophil recruitment in the liver during extrahepatic cholestasis are discussed.
Gulubova
M V
MV
Department of Pathology, Medical Faculty, Trakia University, Stara Zagora, Bulgaria.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001651:Cholestasis, Extrahepatic / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged
D018799:Intercellular Adhesion Molecule-1