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Endotoxin-induced hepatic damage in BCG-infected mice
The American Journal of Pathology
|April 1, 1972
Summary
Mycobacterium BCG infection in mice increases susceptibility to endotoxin, causing acute liver damage. This involves granuloma formation and cellular injury in hepatocytes and liver tissues.
Area of Science:
- Immunology
- Hepatology
- Microbiology
Background:
- Systemic Mycobacterium BCG infection causes liver granulomas in mice.
- BCG infection enhances susceptibility to endotoxin lethality through unknown mechanisms.
Purpose of the Study:
- To investigate the mechanisms underlying enhanced endotoxin susceptibility in BCG-infected mice.
- To characterize the acute hepatic damage induced by endotoxin in the context of BCG infection.
Main Methods:
- Mice were infected systemically with Mycobacterium BCG.
- Endotoxin was administered in small doses to BCG-infected mice.
- Hepatic damage was assessed via serum liver enzymes, light and electron microscopy, and histochemical techniques.
Main Results:
- BCG-infected mice showed elevated serum liver enzymes, indicating acute hepatic damage.
- Morphological alterations included hepatocyte vacuolization, mitochondrial swelling, and endoplasmic reticulum damage.
- Histochemistry revealed acid phosphatase release from granulomas and beta-glucuronidase release from hepatocytes.
Conclusions:
- BCG infection significantly exacerbates endotoxin-induced acute liver injury.
- Endotoxin causes distinct cellular and subcellular damage in the liver of BCG-infected mice.
- The study highlights the complex interplay between mycobacterial infection and endotoxin toxicity in the liver.