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Use of Genetically Altered Mice to Investigate the Role of Nuclear Factor-Kappa B Activation and Cytokine Gene Expression in Sepsis-Induced ARDS*

Timothy S. Blackwell, MD; F.E. Yull; C.-L. Chen; A. Venkatakrishnan; T.R. Blackwell; D.J. Hicks; L.H. Lancaster, MD; J.W. Christman, MD, FCCP; L.D. Kerr
Author and Funding Information

*From Vanderbilt University School of Medicine and the Veterans Affairs Medical Center, Nashville, TN.

Correspondence to: Timothy S. Blackwell, MD, Department of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, T-1217 MCN, Nashville, TN 37232-2650



Chest. 1999;116(suppl_1):73S-74S. doi:10.1378/chest.116.suppl_1.73S
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Production of many inflammatory cytokines and adhesion molecules in vitro is regulated by the ubiquitous transcription factor complex, nuclear factor-kappa B (NF-κB), but the extent to which NF-κB controls specific biological processes in vivo remains unanswered. To examine the function of NF-κB in vivo, we generated a line of transgenic mice expressing Photinusluciferase complementary DNA under the control of an NF-κB-dependent promoter (from the 5′ HIV-1 long terminal repeat). Using these mice, we evaluated NF-κB-dependent luciferase production in a variety of tissues following intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS) at 1 mg/kg. The transgenic animals displayed a time-dependent, organ-specific pattern of NF-κB-dependent luciferase expression, showing that NF-κB activation is induced in multiple organs by systemic LPS administration. Additionally, NF-κB activity in tissue nuclear protein extracts was assayed by electrophoretic mobility shift assay and found to have an organ-specific pattern of activation that correlated well with luciferase activity.


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