Studies on the pathogenesis of rotavirus induced extrahepatic biliary atresia in mice
Date Issued
2003
Date
2003
Author(s)
許宏遠
DOI
912314B002207
Abstract
Recent studies have shown that infection with rhesus rotavirus or group A human rotavirus can induce hepatobiliary inflammation leading to extrahepatic biliary obstruction in newborn BALB/c mice. To understand the role of rotavirus infection in the pathogenesis of extrahepatic biliary atresia (EHBA), rhesus rotavirus (RRV) passaged in MA-104 cells culture and the virus titer determined by plaque assay were done. Primary culture for murine extrahepatic bile duct epithelial cells (MEBEC) were also established. After cocultured with RRV, MEBEC was confirmed to have an expression of the NSP-4 antigen as assessed by immunofluorescence assay (IFA). MEBEC infected with RRV revealed no
obvious cytopathic effect. MEBEC infected by RRV induced a significant decrease in the
absorbance at O.D. 550 nm in a microtiter tetrazolium assay after these treated cells were
cocultured with allogeneic T cells. Our recent study also showed that the expression of ICAM-1 and MHC class I and II antigens on RRV-infected MEBEC were all significantly increased when compared with that of untreated MEBEC. Taken together these findings, we suggest that following upregulation of surface MHC antigens and adhesion molecules with cytokine treatment or RRV infection, the MEBEC can trigger the recognition of MEBEC by effector-T cell mediated cytotoxic responses. Our studies are ongoing to determine whether RRV-infected MEBEC can induce T cell proliferation. These data are important in
understanding the possible role of rotavirus infection in immune-mediated biliary epithelial
cell injury disorders.
Subjects
Rotavirus
MHC antigens
intercellular adhesion molecule
murine extrahepatic
bile duct cell
bile duct cell
proliferation
cytotoxicity
Publisher
臺北市：國立臺灣大學醫學院一般醫學科
Type
journal article
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