Abstract
Whether immunological responses are involved in initiation and progression of alcoholic liver disease is unclear. We describe a mouse model of alcoholic liver injury characterized by steatosis and hepatic inflammation initiated by a recall immune response. Mice immune to Listeria monocytogenes fed a liquid diet containing ethanol and challenged with viable bacteria developed steatosis within 24 h and, at a later time, elevated serum alanine aminotransferase levels, indicating more liver damage in this group. Listeria antigen also induced steatosis and increased serum alanine aminotransferase levels in immune ethanol-consuming mice. The production of tumour necrosis factor by a recall immune response in this model is a major, but not the only, component in initiation of alcoholic liver disease.
Original language | English (US) |
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Pages (from-to) | 123-133 |
Number of pages | 11 |
Journal | Clinical and Experimental Immunology |
Volume | 125 |
Issue number | 1 |
DOIs | |
State | Published - 2001 |
Keywords
- Alcoholic liver disease
- Hepatitis
- Immunopathology
- Steatosis
ASJC Scopus subject areas
- General Medicine