HBV precore mutants and response to interferon

It seemed likely that the expression of ICAM-1 on isolated To the Editor: hepatocytes resulted from the advent on the cell surface of antigen sites of ICAM-1, which has been masked by cell-toIn a 1995 issue of HEPATOLOGY, van Oosten et al. reported cell contact in the liver, possibly, as a consequence of conforon the quantitative expression of vascular adhesion moleculemational changes of ICAM-1 protein in the plasma mem1 and of intercellular adhesion molecule-1 (ICAM-1) on liver brane during dissociation procedure. Recently, Loyer et al. parenchymal and nonparenchymal cells that were isolated reported that hepatocytes at the G0/G1 transition and followfrom rats given lipopolysaccharide using labeled antibodies. ing cell-to-cell contact disruption expressed several early Their observations regarding ICAM-1 expression were as folgenes. This possibility should be also considered. lows: 1) hepatocytes, as well as nonparenchymal cells, However, we feel that it may be necessary to check the showed a basal expression of ICAM-1, although the expresupregulation of ICAM-1 expression on liver cells, especially sion on sinusoidal endothelial cells in untreated rats was two on hepatocytes, with liver tissue specimens of lipopolysacchatimes higher than that on hepatocytes and Kupffer cells; and ride-treated rats before the authors concluded the signifi2) stimulation with lipopolysaccharide increased the exprescance of adhesion molecule expression in the development of sion of ICAM-1 2.5 times for hepatocytes and approximately liver injury during septic shock. 4 times for endothelial cells and Kupffer cells. The authors concluded that such upregulation of ICAM-1 expression on hepatocytes following lipopolysaccharide adSATOSHI MOCHIDA, M.D., Ph.D. Third Department of Internal Medicine ministration may be a contributing factor to the influx of leukocytes and the liver tissue damage during septic shock. Saitama Medical School Saitama, Japan The observations are interesting, but we are concerned about the conclusions drawn by them, because adhesion molecule expression on isolated rat liver cells may not always reflect AKIHIKO OHNO, M.D. Third Department of Internal Medicine, the in vivo state. Recently, we demonstrated that lipopolysaccharide adminSaitama Medical School, Saitama, Japan and First Department of Internal Medicine, Faculty of Medicine istration increased immunohistochemical expressions of ICAM-1 and lymphocyte function-associated antigen 1 on heUniversity of Tokyo Tokyo, Japan patic sinusoidal endothelial cells and macrophages, respectively; that was accomplished in Propionibacterium acnespretreated rats, leading to massive hepatic necrosis through KENJI FUJIWARA, M.D., Ph.D. Third Department of Internal Medicine the microcirculatory disturbance due to sinusoidal coagulopathy initiated by both cell adhesion via these adhesion moleSaitama Medical School Saitama, Japan cules. In such rats, the upregulation of ICAM-1 expression on the endothelial cells increased with a transient elevation REFERENCES of serum tumor necrosis factor a levels, but the ICAM-1 expression on hepatocytes was not seen throughout the pe1. van Oosten M, van de Bilt E, de Vries HE, van Berkel ThJC, Kuiper J. Vascular adhesion molecule-1 and intercellular adhesion molecule-1 expresriod towards hepatic necrosis. sion on rat liver cells after lipopolysaccharide administration in vivo. HEPAThe ICAM-1 expression was also immunohistochemically TOLOGY 1995;22:1538-1546. detected on sinusoidal endothelial cells but not on hepato2. Mochida S, Ohno A, Arai M, Tamatani T, Miyasaka M, Fujiwara K. Role of adhesion molecules in the development of massive hepatic necrosis in cytes in normal rats, suggesting that ICAM-1 expression on rats. HEPATOLOGY 1996;23:320-328. hepatocytes in vivo is different from the expression on iso3. Arai M, Mochida S, Ohno A, Ogata I, Fujiwara K. Sinusoidal endothelial lated hepatocytes. Moreover, the expression of ICAM-1 on cell damage by activated hepatic macrophages in rat liver necrosis. Gastrohepatocytes became detectable even in normal liver when enterology 1993;104:1466-1471. 4. Ohno A, Mochida S, Arai M, Fujiwara K.ICAM-1 expression in hepatocytes the cells were detached from adjacent hepatocytes through following dissociation of cell-to-cell contact in rats. Biochem Biophys Res perfusion with Hank’s balanced salt solution at a threefold Commun 1995;214:1225-1231. physiological flow rate or with collagenase or EGTA. Also, 5. Loyer P, Cariou S, Glaise D, Bilodeau M, Baffet G, Guguen-Guillouzo C. this expression was not affected by cycloheximide at a suffiGrowth factor dependence of progression through G1 and S phases of adult rat hepatocytes in vitro. J Biol Chem 1996;271:11484-11492. cient concentration to inhibit the synthesis of ICAM-1.