Abstract
This chapter reviews the current concept of Kupffer cell-mediated liver injury and the way it relates to the hypothesis on the mechanism by which Alcoholic Liver Disease (ALD) is caused, and several key issues that have to be addressed in this field. These issues include: the way Kupffer cells undergo priming and activation during ALD, the kinds of mediators that are involved, can gender difference in susceptibility to ALD be explained by the concept, and the way a concept translates into a strategy for therapeutics of ALD. The hepatotoxic effects of alcohol are described in detail, but mechanisms underlying the hepatotoxicity have only partially been characterized. Recently, increasing lines of evidence indicate that Kupffer cells play multiple roles in initiation and progression of ALD. After ethanol exposure, Kupffer cells are activated via a mechanism dependent on gut-derived endotoxin, and release active mediators—such as proinflammatory cytokines, eicosanoides, and reactive oxygen intermediates. These mediators are responsible for the pathophysiology of alcoholic liver disease.
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