Department of Pediatric Surgery, Hirosaki University School of Medicine and Hospital
Department of Vascular Biology, Hirosaki University Graduate School of Medicine
Department of Vascular Biology, Hirosaki University Graduate School of Medicine
Department of Vascular Biology, Hirosaki University Graduate School of Medicine
Department of Vascular Biology, Hirosaki University Graduate School of Medicine
Department of Gastroenterology and Hematology,Hirosaki University Graduate School of Medicine
Department of Vascular Biology, Hirosaki University Graduate School of Medicine
Department of Pediatric Surgery, Hirosaki University School of Medicine and Hospital
Department of Pediatric Surgery, Hirosaki University School of Medicine and Hospital
Department of Pathology and Molecular Medicine,Hirosaki University Graduate School of Medicine
Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
Department of Pediatric Surgery, Hirosaki University School of Medicine and Hospital
抄録
Purpose: Retinoic acid-inducible gene-I (RIG-I) is a member of cytoplasmic viral sensors which plays an important role in inflammation of biliary epithelial cells( BECs). The aim of this study is to examine if RIG-I and C-X-C motif chemokine 10( CXCL10) are involved in the etiology of human biliary atresia( BA).
Methods: Immunohistochemical study was performed on surgically resected tissues obtained( June 1994 to March 2016)from 30 infants with BA and non-inflamed hepatic tissues from 7 infants with hepatoblastoma. A semiquantitative scoring system was designed to evaluate the staining with an antibodies to the RIG-I and CXCL10. The expression of RIG-I and CXCL10 in HuCCT1 cholangiocarcinoma cell line were studied by western blotting, ELISA and RT-PCR analyses.
Results: Intense immunoreactivity for RIG-I and CXCL10 was detected in BECs in tissues resected from BA patients.The expression of RIG-I and CXCL10 in the hilar tissue was significantly stronger than in the hepatic tissue.Transfection of HuCCT1 cells with poly(I:C), a synthetic analog of viral dsRNA, induced the expression of RIG-I, and knockdown of RIG-I inhibited the induction of CXCL10 in HuCCT1 cells transfected with poly(I:C).
Conclusion: These results suggest that RIG-I-CXCL10 cascade may be involved in the etiology of human BA.