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Am. J. Respir. Crit. Care Med., Volume 162, Number 3, September 2000, 1095-1101

Multiorgan Nuclear Factor Kappa B Activation in a Transgenic Mouse Model of Systemic Inflammation

TIMOTHY S. BLACKWELL, FIONA E. YULL, CHIH-LI CHEN, ANNAPURNA VENKATAKRISHNAN, THOMAS R. BLACKWELL, DONNA J. HICKS, LISA H. LANCASTER, JOHN W. CHRISTMAN, and LAWRENCE D. KERR

Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Departments of Microbiology and Immunology, and Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; and Department of Veterans Affairs Medical Center, Nashville, Tennessee

We utilized a line of transgenic mice expressing Photinus luciferase complementary DNA (cDNA) under the control of a nuclear factor kappa B (NF-kappa B)-dependent promoter (from the 5' human immunodeficiency virus-1 [HIV-1] long terminal repeat) to examine the role of NF-kappa B activation in the pathogenesis of systemic inflammation induced by bacterial endotoxin (lipopolysaccharide [LPS]). After intraperitoneal injection of E. coli LPS, these mice displayed a time- and dose-dependent, organ-specific pattern of luciferase expression, showing that NF-kappa B-dependent gene transcription is transiently activated in multiple organs by systemic LPS administration. Luciferase expression in liver could be specifically blocked by intravenous administration of replication-deficient adenoviral vectors expressing a dominant inhibitor of NF-kappa B (Ikappa B-alpha DN), confirming that luciferase gene expression is a surrogate marker for NF-kappa B activation in this line of mice. After treatment with intraperitoneal LPS, the mice were found to have increased lung tissue messenger RNA (mRNA) expression of a variety of cytokines that are thought to be NF-kappa B-dependent, as well as elevated serum concentrations of presumed NF-kappa B-dependent cytokines. In lung tissue homogenates, a close correlation was identified between luciferase activity and KC levels. These studies show that systemic treatment with LPS orchestrates a multiorgan NF-kappa B-dependent response that likely regulates the pathobiology of systemic inflammation.




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