| Autor: |
Batey, R., Cao, Q., Madsen, G., Pang, G., Russell, A., Clancy, R. |
| Zdroj: |
Alcoholism: Clinical and Experimental Research; February 1998, Vol. 22 Issue: 1 p150-156, 7p |
| Abstrakt: |
The relationship between the changes in liver pathology and the production of interleukin (IL)‐1α, IL‐6, and tumor necrosis factor‐α (TNF‐α) by intrahepatic mononuclear cells was studied in rats fed alcohol and subsequently exposed to lipopolysaccharide (LPS). Rats were fed 40% ethanol in drinking water, whereas control rats were provided with a chow diet with isocaloric or 2% sucrose drinking solutions for up to 20 weeks. Decreased IL‐1α and TNF‐α production in 24‐hr culture supernatants of mononuclear cells isolated from liver perfusate was detected while IL‐6 remained unchanged over 20 weeks. When animals were injected with LPS (1.0 μg/kg body weight), there was a 5‐fold rise in ALT levels in the ethanol‐fed group, but not in control groups. Increased IL‐6 and TNF‐α levels in the serum and supernatant of cultured intrahepatic mononuclear cells stimulated with or without LPS or concanavalin A was observed. There was a correlation between levels of ALT and TNF‐α, but not IL‐6. T cells and Kupffer cells were the major source of TNF‐α in culture supernatants of hepatic perfusate mononuclear cells from ethanol‐consuming rats injected LPS. In addition, pathological liver injury was evident, which suggests a pathogenic role for TNF‐α in alcohol‐induced liver disease. |
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