title: Induction of autoimmune-like hepatic and ductal lesions by administration of lipopolysaccharide in mice undergoing graft-versus-host reaction across MHC class I difference.
abstract: In this paper, we examined the induction of autoimmune-like histologic changes in the liver and other organs of mice undergoing graft-versus-host reaction (GVHR) with MHC class I disparity by the administration of bacterial lipopolysaccharide (LPS), on the assumption that stimulation with LPS could be an exacerbating factor. Spleen cells of C57BL/6 (B6) mice were injected twice into (B6 x bml) F1 recipient mice at an interval of 7 days to induce MHC class I GVHR and then challenged with 1 microg of LPS intravenously on the next day of the cell transfer. The hepatic lesions of the group of MHC class I GVHR mice challenged with LPS showed marked cellular infiltration at the portal area and focal necrosis was observed in the hepatic lobule. The major infiltrating cells were CD8+, and others including CD4+ cells being of minor populations. In addition, ductal lesions in extrahepatic organs, including the pancreas and salivary glands also showed marked cellular infiltration. Thus, we have demonstrated that LPS induced ductal lesions in mice with MHC class I disparity. CD8+ cells were detected at the destructive hepatic lesions, which might be effector cells. These findings indicate that LPS might be one of the potential factors which augment autoimmune-like lesions.
authors.affiliation: Animal Center for Biomedical Research, Faculty of Medicine, The University of Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Hayashi
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Narita
authors.forename: R
authors.initials: R
authors.lastname: Yui
authors.forename: S
authors.initials: S
authors.lastname: Inada
authors.forename: T
authors.initials: T
authors.lastname: Kimura
authors.forename: Y
authors.initials: Y
authors.lastname: Aizawa
authors.forename: M
authors.initials: M
authors.lastname: Zeniya
authors.forename: G
authors.initials: G
authors.lastname: Toda
authors.forename: M
authors.initials: M
authors.lastname: Fujiwara
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology*; D001652:Bile Ducts / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology; D056486:Chemical and Drug Induced Liver Injury; D006087:Graft vs Host Reaction / Q000276:immunology*; D006183:H-2 Antigens / Q000096:biosynthesis / Q000276:immunology; D006503:Hepatic Veins / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006529:Hepatomegaly; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000276:immunology*; D008107:Liver Diseases / Q000276:immunology*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D011169:Portal Vein / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013163:Splenomegaly
chemical_list: D006183:H-2 Antigens; C032876:H-2Kb protein, mouse; D015395:Histocompatibility Antigens Class I; D008070:Lipopolysaccharides; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1; D000410:Alanine Transaminase