Ferrante A, Carter R F, Ferluga J, Allison A C
Infect Immun. 1984 Nov;46(2):501-6. doi: 10.1128/iai.46.2.501-506.1984.
Rats and mice infected with Trypanosoma lewisi and Trypanosoma musculi, respectively, showed hyperreactivity to lipopolysaccharide (LPS) from gram-negative bacteria. Fatal shock could be precipitated with a dose of LPS 100 to 1,000 times less in infected compared with noninfected animals. In trypanosome-infected rats and mice, extensive liver damage was evident after LPS challenge. These animals showed a pronounced hypoglycemia, marked elevation of blood aspartate transaminase level, and diffuse severe degeneration and total depletion of glycogen in hepatocytes. Only minor changes were observed in noninfected animals given the same dose of LPS. No mononuclear phagocytic cell infiltration was observed in the liver of infected animals. The most striking change was the great increase in size and the probable increase in phagocytic activity and number of sinusoidal Kupffer cells. We suggest that elevated Kupffer cell activity in trypanosome-infected animals may play a role in LPS-induced hepatotoxicity.
分别感染了刘易斯锥虫和鼠锥虫的大鼠和小鼠,对革兰氏阴性菌的脂多糖(LPS)表现出反应过度。与未感染动物相比,感染动物用剂量低100至1000倍的LPS就能引发致命性休克。在锥虫感染的大鼠和小鼠中,LPS激发后肝脏出现广泛损伤。这些动物表现出明显的低血糖、血液中天冬氨酸转氨酶水平显著升高,以及肝细胞中糖原弥漫性严重变性和完全耗竭。给予相同剂量LPS的未感染动物仅观察到轻微变化。在感染动物的肝脏中未观察到单核吞噬细胞浸润。最显著的变化是肝血窦枯否细胞的大小大幅增加,吞噬活性和数量可能也增加。我们认为,锥虫感染动物中枯否细胞活性升高可能在LPS诱导的肝毒性中起作用。