Lymphotoxin-beta production following bile duct ligation: Possible role for Kupffer cells
Lee, C.M., Knight, B., Yeoh, G.C., Ramm, G.A. and Olynyk, J.K. (2005) Lymphotoxin-beta production following bile duct ligation: Possible role for Kupffer cells. Journal of Gastroenterology and Hepatology, 20 (11). pp. 1762-1768.
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Background and Aims: Lymphotoxin-β (LT-β) may play a role in the pathogenesis of chronic liver injury. The aim of this study was to determine in an animal model of bile duct ligation liver injury whether LT-β expression is induced and whether Kupffer cells are an intrahepatic source of LT-β.
Methods: Sprague–Dawley rats were divided into two groups: one group received a single dose of GdCl (a Kupffer cell-blocking agent, 10 mg/kg i.v.), whereas the other group received saline. One day later, the groups underwent bile duct ligation or a sham operation. Liver tissue was obtained on days 1, 3, 5, and 8 for assessment of Kupffer cell numbers, early fibrogenic events and LT-β gene expression. Kupffer cells were isolated using pronase/collagenase perfusion and centrifugal elutriation.
Results: Hepatic LT-β mRNA expression increased early following bile duct ligation. Pretreatment of bile duct-ligated animals with GdCl significantly reduced the number of Kupffer cells, delayed the rise in LT-β expression, but had no effect on fibrogenesis. Recovery of the Kupffer cell population in these animals was accompanied by increased hepatic LT-β expression. The LT-β ligand and receptor were expressed by isolated normal Kupffer cells.
Conclusions: Hepatic LT-β expression is induced early following bile duct ligation. Kupffer cells may be an intrahepatic source of LT-β.
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|Copyright:||© 2005 Blackwell Publishing Asia Pty Ltd|
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