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B, and TNF-
1 Laboratory of Hepatobiology and Toxicology, Department of Pharmacology and 3 Department of Pathology, University of North Carolina, Chapel Hill, North Carolina 27599-7365; and 2 Department of Medicine, University of Southern California, Los Angeles, California 90033
The purpose of
this study was to determine whether early alcohol-induced liver injury
(ALI) in females is associated with changes in CD14 on Kupffer cells,
activation of hepatic nuclear factor (NF)-
B, and expression of tumor
necrosis factor (TNF)-
mRNA. Male and female rats were given
high-fat control or ethanol-containing diets for 4 wk using the
intragastric enteral protocol. Physiological parameters were similar in
both genders. Ethanol was increased as tolerance developed with higher
blood levels than previously observed, resulting in a fourfold increase
in aspartate aminotransferase (males 389 ± 47 IU/l vs. females 727 ± 66 IU/l). Hepatic pathology developed more rapidly and was nearly
twofold greater and endotoxin levels were significantly higher in
females after ethanol. Also, expression of CD14 on Kupffer cells was
1.5-fold greater and binding of transcription factor NF-B in hepatic
nuclear extracts and TNF- mRNA expression were threefold greater in
females. These data are consistent with the hypothesis that elevated
endotoxin after ethanol triggers more activation of Kupffer cells via
enhanced CD14 expression in females. NF-B is activated in this
process, leading to increases in TNF- mRNA expression in the liver
and more severe liver injury in females. It is concluded that gender differences in ALI are dependent on endotoxin and a signaling cascade
leading to TNF-.
Kupffer cells; endotoxin
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