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David A. Geller, MD; Paul H. Kispert, MD; Grace L. Su, MD; Stewart C. Wang, MD; Mauricio Di Silvio, MD; David J. Tweardy, MD; Timothy R. Billiar, MD; Richard L. Simmons, MD

Arch Surg. 1993;128(1):22-28.

Abstract
• 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, Corynebacteriumparvum, 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.

(Arch Surg. 1993;128:22-28)

Author Affiliations
From the Departments of Surgery (Drs Geller, Kispert, Su, Wang, Di Silvio, Billiar, and Simmons) and Medicine (Drs Su and Tweardy), University of Pittsburgh (Pa).

Footnotes
Accepted for publication September 20, 1992.

Presented at the 12th Annual Meeting of the Surgical Infection Society, Los Angeles, Calif, April 9, 1992.

Reprints not available.

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