title: Increase of chemokine interferon-inducible protein-10 (IP-10) in the serum of patients with autoimmune liver diseases and increase of its mRNA expression in hepatocytes.
abstract: To clarify the role of IP-10 in autoimmune liver diseases, we studied the serum levels of IP-10 in 14 patients with autoimmune hepatitis (AIH), 23 patients with primary biliary cirrhosis (PBC), and 65 patients with chronic viral hepatitis (20 type B and 45 type C). The hepatic expression of IP-10 mRNA and the correlation between the serum levels of IP-10 and clinical parameters were also evaluated. In addition to 20 healthy controls, 16 rheumatoid arthritis (RA) patients were included as an extrahepatic inflammatory disease. The serum level of IP-10 was significantly (P < 0.02) higher in patients with AIH, PBC, and chronic hepatitis B and C than in healthy controls, and it was significantly correlated (P < 0.05) with the serum levels of aspartate aminotransferase and alanine aminotransferase in patients with AIH, PBC, and chronic hepatitis B and C. The serum level of IP-10 was not elevated in RA patients. After successful treatment of AIH and chronic hepatitis C, the serum level of IP-10 decreased to the same level as in healthy volunteers. As we previously showed in cases with chronic hepatitis B or C, in situ hybridization in both AIH and PBC cases demonstrated the expression of IP-10 mRNA in hepatocytes around focal or lobular necrosis surrounded by infiltrating mononuclear cells, whereas IP-10 mRNA was not expressed in areas around the damaged bile ducts in PBC cases. The present results suggest that IP-10 is specifically produced by hepatocytes in inflammatory areas irrespective of the aetiology of hepatitis, and that IP-10 may help to recruit T cells to the hepatic lesions in autoimmune liver diseases as well as in chronic viral hepatitis.
authors.affiliation: Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nishioji
authors.forename: T
authors.initials: T
authors.lastname: Okanoue
authors.forename: Y
authors.initials: Y
authors.lastname: Itoh
authors.forename: S
authors.initials: S
authors.lastname: Narumi
authors.forename: M
authors.initials: M
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
authors.forename: A
authors.initials: A
authors.lastname: Morita
authors.forename: K
authors.initials: K
authors.lastname: Kashima
mesh_terms: D001327:Autoimmune Diseases / Q000097:blood* / Q000276:immunology; D001483:Base Sequence; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood* / Q000235:genetics / Q000276:immunology; D006801:Humans; D008099:Liver / Q000276:immunology / Q000378:metabolism; D008107:Liver Diseases / Q000097:blood* / Q000276:immunology; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics
chemical_list: D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D012333:RNA, Messenger