| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print October 15, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00253.2001
Submitted on June 14, 2001
Accepted on October 10, 2001
1 Medicine, University of Michigan, Ann Arbor, MI, USA; Veterans Administration Health Systems, Ann Arbor, MI, USA
2 North Shore University Hospital/NYU School of Medicine, Manhasset, NY, USA
3 Surgery, University of Michigan, Ann Arbor, MI, USA
4 Medicine, University of Michigan, Ann Arbor, MI, USA
5 Pathology, University of Michigan, Ann Arobr, MI, USA
* To whom correspondence should be addressed. E-mail: gsu{at}umich.edu.
Upregulation of CD14 in Kupffer cells has been implicated in the pathogenesis of several forms of liver injury including alcoholic liver disease. However, it remains unclear whether CD14 mediates lipopolysaccharide (LPS) signaling in this specialized liver macrophage population. In this series of experiments, we determined the role of CD14 in LPS activation of Kupffer cells by using several complementary approaches. First, we isolated Kupffer cells from human livers and studied the effects of anti-CD14 antibodies on LPS activation of these cells. Kupffer cells were incubated with increasing concentrations of LPS in the presence and absence of recombinant human LPS binding protein (LBP). With increasing concentrations of LPS, human Kupffer cell TNF-
production (a marker for Kupffer cell activation) increased in a dose dependent manner in the presence and absence of LBP. In the presence of anti-human CD14 antibodies, the production of TNF- was significantly diminished. Second, we compared LPS activation of Kupffer cells isolated from wildtype and CD14 knockout mice. Kupffer cells from CD14 knockout mice produced significantly less TNF- in response to the same amount of LPS. Taken together, this data strongly supports a critical role for CD14 in Kupffer cell responses to LPS.
This article has been cited by other articles:
|
|
 |
|
  B. Vollmar and M. D. Menger The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair Physiol Rev, October 1, 2009; 89(4): 1269 - 1339. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Minter, X. Bi, G. Ben-Josef, T. Wang, B. Hu, S. Arbabi, M. R. Hemmila, S. C. Wang, D. G. Remick, and G. L. Su LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction Am J Physiol Gastrointest Liver Physiol, January 1, 2009; 296(1): G45 - G54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Levy, J. M. Prince, R. Yang, K. P. Mollen, H. Liao, G. A. Watson, M. P. Fink, Y. Vodovotz, and T. R. Billiar Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4 Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2006; 291(4): R970 - R976. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Uchikura, T. Wada, S. Hoshino, Y. Nagakawa, T. Aiko, G. B. Bulkley, A. S. Klein, and Z. Sun Lipopolysaccharides induced increases in Fas ligand expression by Kupffer cells via mechanisms dependent on reactive oxygen species Am J Physiol Gastrointest Liver Physiol, September 1, 2004; 287(3): G620 - G626. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
