Funaki N, Arii S, Monden K, Sasaoki T, Adachi Y, Higashitsuji H, Tanaka J, Imamura M
First Department of Surgery, Faculty of Medicine, Kyoto University, Japan.
Life Sci. 1994;54(26):2071-82. doi: 10.1016/0024-3205(94)00716-0.
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.
本研究旨在分析四氯化碳（CCl4）诱导的肝硬化大鼠肝巨噬细胞（HM phi）可能的功能改变。给大鼠注射CCl4 13周后培养24小时，其HM phi释放的前列腺素E2（PGE2）和肿瘤坏死因子（TNF）量低于正常水平，而白细胞介素-1（IL-1）释放量非常大。给大鼠注射CCl4 9周时，仅PGE2生成减少。9周和13周组HM phi上白细胞介素-2受体（IL-2R）、Ia抗原和去唾液酸GM1抗原的表达均显著降低。13周组IL-2R和Ia抗原表达下降幅度更大。因此，得出结论，随着肝硬化进展，源自CCl4诱导的肝硬化肝脏的HM phi在细胞因子释放（IL-1除外）方面表现出功能改变，且表面标志物表达降低。这些结果应为进一步研究肝硬化存在时宿主受损状态提供依据。
