Fukuda I, Tanamoto K, Kanegasaki S, Yajima Y, Goto Y
Institute of Medical Science, University of Tokyo, Japan.
Br J Exp Pathol. 1989 Jun;70(3):267-74.
The possible role of liver parenchymal cells in the uptake and degradation of bacterial lipopolysaccharide (LPS) was investigated in vitro by employing radiolabelled LPS as substrate. Hepatocytes obtained from Wistar rats by collagenase treatment were found to take up LPS only when it was not linked to the polysaccharide of O-antigen. The amount of LPS taken up increased with time and after 48 h incubation it increased in a dose-dependent manner up to at least 30 micrograms. When incubated with LPS radiolabelled exclusively in the fatty-acid moiety, cultured hepatocytes released lipophilic materials into the culture medium. These were identified as beta-hydroxytetradecanoic acid and triglyceride, in the ratio of 7:I. These results indicate that the R-form of LPS which lacks the O-antigen polysaccharide is taken up and deacylated in hepatocytes, and the derived fatty acids are released into the culture medium either in the free form or after conversion to triglyceride.
通过使用放射性标记的脂多糖（LPS）作为底物，在体外研究了肝实质细胞在摄取和降解细菌脂多糖（LPS）中的可能作用。通过胶原酶处理从Wistar大鼠获得的肝细胞仅在LPS未与O抗原多糖连接时才摄取它。摄取的LPS量随时间增加，孵育48小时后，其以剂量依赖性方式增加，至少增加至30微克。当与仅在脂肪酸部分放射性标记的LPS一起孵育时，培养的肝细胞将亲脂性物质释放到培养基中。这些被鉴定为β-羟基十四烷酸和甘油三酯，比例为7:1。这些结果表明，缺乏O抗原多糖的LPS的R形式在肝细胞中被摄取并脱酰基，并且衍生的脂肪酸以游离形式或转化为甘油三酯后释放到培养基中。
