Mizoguchi Y, Kawada N, Tsutsui H, Kobayashi K
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Gastroenterol Jpn. 1993 Mar;28 Suppl 4:30-2; discussion 33-5. doi: 10.1007/BF02782885.
When heat-killed Propionibacterium acnes (P. acnes) was intravenously injected into mice and 7 days later a small amount of lipopolysaccharide (LPS) endotoxin was administered, most of the mice died of massive liver necrosis. In this liver injury model, cytokines, immunomediators, and eicosanoids, inflammatory products, were produced by Kupffer cells and liver-infiltrated macrophages, which were thought to participate, directly or indirectly, in the induction of liver cell damage. Furthermore, these two networks seemed to regulate each other. Thus, this regulatory mechanism might play an important role in the induction of liver cell injury.
当将热灭活的痤疮丙酸杆菌（P. acnes）静脉注射到小鼠体内，7天后给予少量脂多糖（LPS）内毒素时，大多数小鼠死于大面积肝坏死。在这个肝损伤模型中，细胞因子、免疫介质和类二十烷酸等炎症产物由库普弗细胞和肝脏浸润巨噬细胞产生，这些细胞被认为直接或间接参与肝细胞损伤的诱导。此外，这两个网络似乎相互调节。因此，这种调节机制可能在肝细胞损伤的诱导中起重要作用。
