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Medical Service, Department of Veterans Affairs Medical Center and Department of Medicine, University of Michigan, Ann Arbor, Michigan 48109
Endogenous
gut-derived bacterial lipopolysaccharides have been implicated as
important cofactors in the pathogenesis of liver injury. However, the
molecular mechanisms by which lipopolysaccharides exert their effect
are not entirely clear. Recent studies have pointed to proinflammatory
cytokines such as tumor necrosis factor-
as mediators of hepatocyte
injury. Within the liver, Kupffer cells are major sources of
proinflammatory cytokines that are produced in response to
lipopolysaccharides. This review will focus on three important
molecular components of the pathway by which lipopolysaccharides activate Kupffer cells: CD14, Toll-like receptor 4, and
lipopolysaccharide binding protein. Within the liver,
lipopolysaccharides bind to lipopolysaccharide binding protein, which
then facilitates its transfer to membrane CD14 on the surface of
Kupffer cells. Signaling of lipopolysaccharide through CD14 is mediated
by the downstream receptor Toll-like receptor 4 and results in
activation of Kupffer cells. The role played by these molecules in
liver injury will be examined.
endotoxins; tumor necrosis factor; macrophages; CD14
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