Induction of hepatocyte lipopolysaccharide binding protein in models of sepsis and the acute-phase response
D. A. Geller, P. H. Kispert, G. L. Su, S. C. Wang, M. Di Silvio, D. J. Tweardy, T. R. Billiar and R. L. Simmons
Department of Surgery, University of Pittsburgh, Pa.
Lipopolysaccharide binding protein (LBP) is a serum glycoprotein that
complexes with lipopolysaccharide (LPS) to facilitate macrophage response
to endotoxin. To determine the conditions that stimulate LBP production in
vivo, we measured the induction of LBP in models of inflammation produced
by LPS, Corynebacterium parvum, and turpentine injection. Plasma aspartate
aminotransferase and alanine aminotransferase concentrations and hepatocyte
fibrinogen synthesis were elevated in all models. Northern blot analysis
revealed 17-, 14-, and 20-fold upregulation of hepatocyte LBP mRNA
following treatment with LPS, C parvum, and turpentine, respectively.
Peritoneal macrophage interleukin 6 and tumor necrosis factor production
following endotoxin stimulation was augmented by cultured hepatocyte
supernatants, suggesting increased LBP synthesis in these groups. The
results show that LBP mRNA is induced during hepatic inflammation and
suggest that LBP is an acute-phase protein important in regulating the in
vivo response to endotoxin.
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