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and the TNF-p55 receptor
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)-
. The present study was undertaken to determine whether
membrane-associated or secreted TNF- 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-, the p55 and p75 receptor, and mice expressing
only a cell-associated form of TNF- 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- than any other experimental group (P 
0.05)
and tended to have the highest mortality and liver injury. In contrast,
p55 and TNF- knockout mice and animals expressing only a
cell-associated form of TNF- 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- signaling through the p55 receptor.
apoptosis, hepatitis, septic shock
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