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Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation

Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation Abstract 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-α 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 Footnotes Address for reprint requests and other correspondence: G. L. Su, Univ. of Michigan Medical Center, 1510C MSRB I, Box 0666, 1150 W. Medical Center Dr., Ann Arbor, MI 48109–0666 (E-mail: [email protected] ). 10.1152/ajpgi.00550.2001 Copyright © 2002 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Gastrointestinal and Liver Physiology The American Physiological Society

Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation

Su, Grace L.
AJP - Gastrointestinal and Liver Physiology , Volume 283 (2): G256 – Aug 1, 2002
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References (134)

Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0193-1857
eISSN
1522-1547
DOI
10.1152/ajpgi.00550.2001
pmid
12121871
Publisher site
See Article on Publisher Site

Abstract

Abstract 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-α 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 Footnotes Address for reprint requests and other correspondence: G. L. Su, Univ. of Michigan Medical Center, 1510C MSRB I, Box 0666, 1150 W. Medical Center Dr., Ann Arbor, MI 48109–0666 (E-mail: [email protected] ). 10.1152/ajpgi.00550.2001 Copyright © 2002 the American Physiological Society

Journal

AJP - Gastrointestinal and Liver Physiology – The American Physiological Society

Published: Aug 1, 2002

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