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1 Cardiovascular Institute of the University of Pittsburgh Medical Center Health System, 2 Department of Molecular Genetics and Biochemistry, and 3 Center for Biological Imaging, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213
Tumor necrosis factor (TNF)-
plays a key role in the pathogenesis of septic shock syndrome, and
myocardial TNF- expression may contribute to this pathophysiology.
We examined the myocardial expression of TNF--related cytokines and
chemokines in mice exposed to lipopolysaccharide (LPS) and tested the
effects of anti-TNF therapy on myocardial cytokine expression. Cytokine
mRNA levels were measured by RNase protection assay, and protein levels
in the plasma and myocardium were assessed by enzyme-linked
immunosorbent assays. LPS (4 µg/g body wt ip) induced marked cytokine
expression, including TNF-, interleukin (IL)-1
, IL-6, and
monocyte chemotactic protein (MCP)-1, in both the plasma and
myocardium. Pretreatment with adenovirus-mediated TNF receptor fusion
protein (AdTNFR1; 109 plaque-forming units iv) decreased
plasma cytokine levels. In contrast, whereas myocardial IL-1
expression was also suppressed, expression of IL-6 and MCP-1 was
not inhibited by AdTNFR1. In summary, anti-TNF treatment
differentially altered the cytokine expression in the plasma and
myocardium during endotoxemia. Inability to block myocardial expression
of IL-6 and MCP-1 suggests a possible mechanism for the failure of
anti-TNF therapies in the treatment of endotoxin shock.
adenovirus; chemokine; endotoxin shock; tumor necrosis factor-
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