Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice

I. I. Slukvin, P. J. Boor, T. R. Jerrells

Research output: Contribution to journalArticle

13 Scopus citations

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 languageEnglish (US)
Pages (from-to)123-133
Number of pages11
JournalClinical and Experimental Immunology
Volume125
Issue number1
DOIs
StatePublished - 2001

Keywords

  • Alcoholic liver disease
  • Hepatitis
  • Immunopathology
  • Steatosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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