Endotoxin-induced hepatic damage in BCG-infected mice.

Abstract

Systemic infection of mice with Mycobacterium BCG leads to focal liver damage by producing many granulomas. By undefined mechanisms, this infection markedly enhances the animal's susceptibility to the lethal effect of endotoxin. Small doses of endotoxin given to BCG-infected mice were found to cause acute hepatic damage, as demonstrated by elevated activities of liver enzymes in serum and by morphologic alterations documented by light and electron microscopy and by histochemical technics. The morphologic alterations caused by endotoxin included glycogen depletion, mitochondrial swelling, disruption of the continuity of sinusoidal endothelium and focal injury characterized by marked vacuolization of hepatocytes and distension and fragmentation of rough endoplasmic reticulum. Histochemical studies revealed the apparent release of acid phosphatase from granules in the central portions of granulomas, and the release of beta-glucuronidase from the cytoplasm of hepatocytes.