title: Chemical mediator release and surface marker expression of hepatic macrophages in rats with CCl4-induced liver cirrhosis.
abstract: The present study was performed to analyze possible functional alterations of hepatic macrophages (HM phi) in rats with carbon tetrachloride (CCl4)-induced liver cirrhosis. HM phi from rats injected with CCl4 for 13 weeks and cultured for 24 hours released less than normal amounts of prostaglandin E2 (PGE2) and tumor necrosis factor (TNF) and very large amounts of interleukin-1 (IL-1). In rats injected with CCl4 for 9 weeks, only PGE2 production was reduced. Interleukin-2 receptor (IL-2R), Ia antigen and asialo GM1 antigen expressions on HM phi from both the 9- and 13-week groups were significantly decreased. IL-2R and Ia antigen expressions showed larger decreases in the 13-week group. Thus, it is concluded that HM phi derived from CCl4-induced cirrhotic livers show a functional alteration in the release of cytokines (except for IL-1) and a decrease in surface marker expression, as cirrhosis advances. These results should provide a basis for further investigation into the host-compromised status in the presence of liver cirrhosis.
authors.affiliation: First Department of Surgery, Faculty of Medicine, Kyoto University, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Funaki
authors.forename: S
authors.initials: S
authors.lastname: Arii
authors.forename: K
authors.initials: K
authors.lastname: Monden
authors.forename: T
authors.initials: T
authors.lastname: Sasaoki
authors.forename: Y
authors.initials: Y
authors.lastname: Adachi
authors.forename: H
authors.initials: H
authors.lastname: Higashitsuji
authors.forename: J
authors.initials: J
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Imamura
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000032:analysis; D002252:Carbon Tetrachloride Poisoning / Q000473:pathology / Q000503:physiopathology*; D002469:Cell Separation; D002470:Cell Survival; D002478:Cells, Cultured; D015232:Dinoprostone / Q000096:biosynthesis*; D005677:G(M1) Ganglioside / Q000096:biosynthesis; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis*; D008099:Liver / Q000473:pathology / Q000503:physiopathology*; D008106:Liver Cirrhosis, Experimental / Q000473:pathology / Q000503:physiopathology*; D008264:Macrophages / Q000473:pathology / Q000502:physiology*; D008297:Male; D010587:Phagocytosis; D051381:Rats; D017208:Rats, Wistar; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D000954:Antigens, Surface; D000949:Histocompatibility Antigens Class II; D007375:Interleukin-1; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D005677:G(M1) Ganglioside; C018835:asialo GM1 ganglioside; D015232:Dinoprostone