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production
in rat Kupffer cells after chronic ethanol feeding
Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106-4906
Activation of Kupffer
cells by lipopolysaccharide (LPS) is a critical step in the
pathogenesis of alcoholic liver disease. Kupffer cells isolated from
rats fed ethanol in their diet for 4 wk accumulated 4.3-fold more tumor
necrosis factor (TNF)-
in response to LPS compared with pair-fed
rats. In contrast, LPS-stimulated interleukin (IL)-1 accumulation was
50% lower after ethanol feeding. LPS-stimulated TNF- mRNA
accumulation was twofold higher after ethanol feeding, whereas IL-1
mRNA accumulation was blunted. To understand the mechanisms for this
differential response, we investigated the effects of ethanol on
LPS-dependent signal transduction. Chronic ethanol feeding increased
LPS-stimulated extracellular receptor-activated kinases 1/2 (ERK1/2)
activation. Activation of ERK1/2 was required for maximal increases in
TNF- and IL-1 mRNA and was associated with increased binding of
early growth response-1 (Egr-1) to the TNF- promoter after ethanol
feeding. In contrast, ethanol feeding completely abrogated activation
of nuclear factor-
B DNA-binding activity by LPS and had no effect on
AP-1 binding. Together, these data suggest that enhanced activation of
ERK1/2 and Egr-1 contributes to increased TNF- production after
chronic ethanol feeding.
tumor necrosis factor-; interleukin 1; nuclear factor-B; lipopolysaccharide; macrophage
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