Mizoguchi Y, Kuboi H, Tsutsui H, Seki S, Kobayashi K, Yamamoto S, Morisawa S, Yano I
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Gastroenterol Jpn. 1989 Oct;24(5):519-22. doi: 10.1007/BF02773878.
When BALB/cAJc1 mice are intravenously injected with heat-killed Propionibacterium acnes (P. acnes) followed by an intravenous injection of lipopolysaccharide (LPS) 7 days later, massive necrosis is induced in the liver tissue and most of the mice die within 24 hours of LPS injection. Using this experimental model, acute hepatic failure was induced in various strains of mice and the difference in the response was studied. As a result, as in BALB/cAJc1 mice, acute hepatic failure was also induced in BALB/cAJc1-nu, AKR/J, C3H/HeNJc1, C57BL/6NJc1 and DDy mice. However, as an exception, hepatic cell necrosis was hardly seen and the survival rate was remarkable high in C3H/HeJ mice, which genetically do not respond to LPS stimulation. These results indicate that for this experimental induction of acute hepatic failure, macrophages must be activated by the two-step stimulation of P. acnes and LPS.
当给BALB/cAJc1小鼠静脉注射热灭活的痤疮丙酸杆菌（P. acnes），并在7天后静脉注射脂多糖（LPS）时，肝组织会诱导出大量坏死，且大多数小鼠在注射LPS后的24小时内死亡。利用该实验模型，在各种品系的小鼠中诱导出急性肝衰竭，并研究了反应差异。结果，与BALB/cAJc1小鼠一样，BALB/cAJc1-nu、AKR/J、C3H/HeNJc1、C57BL/6NJc1和DDy小鼠也诱导出了急性肝衰竭。然而，作为例外，在基因上对LPS刺激无反应的C3H/HeJ小鼠中，几乎未见肝细胞坏死，存活率显著较高。这些结果表明，对于这种急性肝衰竭的实验诱导，巨噬细胞必须通过痤疮丙酸杆菌和LPS的两步刺激而被激活。
