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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00328.2001
Submitted on July 27, 2001
Accepted on September 1, 2001
production in rat Kupffer cells after chronic ethanol feeding
1 Nutrition, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: len2{at}po.cwru.edu.
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 weeks accumulated 4.3-fold more tumor necrosis factor (TNF) in response to LPS compared to pair-fed rats. In contrast, LPS-stimulated IL-1 accumulation was 50% lower after ethanol feeding. LPS-stimulated TNF mRNA accumulation was 2-fold higher after ethanol feeding, while IL-1ß mRNA accumulation was blunted. In order 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 ERK1/2 activation. Activation of ERK1/2 was required for maximal increases in TNF and IL-1ß mRNA and was associated with increased binding of Egr-1 to the TNF promoter after ethanol feeding. In contrast, ethanol feeding completely abrogated activation of NF
B DNA binding activity by LPS and had no effect on AP-1 binding. Taken together, these data suggest that enhanced activation of ERK1/2 and Egr-1 contributes to increased TNF production after chronic ethanol feeding.
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