Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice.
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.
Slukvin
I I
II
Department of Cellular Biology and Anatomy, Louisiana State University Medical Center, Shreveport, LA, USA.
Boor
P J
PJ
Jerrells
T R
TR
D000410:Alanine Transaminase / Q000097:blood; D000428:Alcohol Drinking / Q000276:immunology*; D000818:Animals; D004195:Disease Models, Animal; D005235:Fatty Liver, Alcoholic / Q000097:blood / Q000276:immunology*; D005260:Female; D008089:Listeria monocytogenes / Q000276:immunology; D008088:Listeriosis / Q000276:immunology*; D008099:Liver / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D014409:Tumor Necrosis Factor-alpha; D000410:Alanine Transaminase