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Am J Physiol Regul Integr Comp Physiol 278: R1202-R1209, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 5, R1202-R1209, May 2000

LPS-induced liver injury in D-galactosamine-sensitized mice requires secreted TNF-alpha and the TNF-p55 receptor

Monika Nowak1, Gregory C. Gaines1, Jason Rosenberg1, Rebecca Minter1, F. R. Bahjat1, John Rectenwald1, Sally L. D. MacKay1, Carl K. Edwards III2, and Lyle L. Moldawer1

1 Department of Surgery, University of Florida College of Medicine, Gainesville, Florida 32610; and 2 Amgen, Thousand Oaks, California 91320

Lipopolysaccharide and D-galactosamine induced lethality and apoptotic liver injury is dependent on endogenously produced tumor necrosis factor (TNF)-alpha . The present study was undertaken to determine whether membrane-associated or secreted TNF-alpha signaling through the p55 or p75 receptor was responsible for survival and hepatic injury after lipopolysaccharide administration in D-galactosamine-sensitized mice. Transgenic mice expressing null forms of TNF-alpha , the p55 and p75 receptor, and mice expressing only a cell-associated form of TNF-alpha were challenged with 8 mg D-galactosamine and 100 ng lipopolysaccharide. Mortality and apoptotic liver injury were only seen in wild-type and p75 knockout mice. p75 Knockout mice had significantly higher concentrations of plasma TNF-alpha than any other experimental group (P <=  0.05) and tended to have the highest mortality and liver injury. In contrast, p55 and TNF-alpha knockout mice and animals expressing only a cell-associated form of TNF-alpha exhibited no mortality or liver injury. We conclude that survival and apoptotic liver injury in response to lipopolysaccharide and D-galactosamine are dependent exclusively on secreted TNF-alpha signaling through the p55 receptor.

apoptosis, hepatitis, septic shock


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