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Inhibition of endotoxin-induced lung inflammation by interleukin-10 gene transfer in mice.

Authors
Dokka-S; Malanga-CJ; Shi-X; Chen-F; Castranova-V; Rojanasakul-Y
Source
Am J Physiol, Lung Cell Mol Physiol 2000 Nov; 279(5):L872-L877
NIOSHTIC No.
20020654
Abstract
Interleukin (IL)-10 is an anti-inflammatory cytokine that has great potential for use in the treatment of inflammatory and immune illnesses. In this study, gene transfer was used to induce IL-10 transgene expression in murine lungs for treatment of endotoxin-induced lung inflammation. Gene transfer was performed with a cytomegalovirus (CMV)-IL-10 plasmid with the aid of the liposomal agents LipofectAMINE and N-[1-(2,3-dioleoyl)propyl]-N,N, N-trimethylammonium methylsulfate (DOTAP). Administration of the endotoxin caused a marked increase in lung inflammation as indicated by increased tumor necrosis factor (TNF)-alpha release and neutrophil count. Pretreatment of the mice with IL-10 plasmid with and without LipofectAMINE had no inhibitory effect on lung inflammation and IL-10 transgene expression. LipofectAMINE by itself induced lung inflammation, an effect that was not observed with DOTAP. IL-10 plasmid when codelivered with DOTAP expressed biologically active IL-10 protein and caused a reduction in endotoxin-induced inflammation. Transgene expression was observed as early as 3 h after administration, peaked at 12 h, and declined thereafter. We conclude that IL-10 gene transfer is a feasible approach for the treatment of lung inflammation.
Keywords
Endotoxins; Laboratory-animals; Animals; Animal-studies; Lung-disorders; Lung-irritants; Pulmonary-system-disorders; Respiratory-system-disorders
Contact
Y. Rojanasakul, West Virginia University School of Pharmacy, Department of Basic Pharmaceutical Sciences, PO Box 9530, Morgantown, WV 26506
CODEN
APLPE7
Publication Date
20001101
Document Type
Journal Article
Email Address
yrojanasakul@hsc.wvu.edu
Fiscal Year
2001
NTIS Accession No.
NTIS Price
Issue of Publication
5
ISSN
1040-0605
NIOSH Division
HELD
Source Name
American Journal of Physiology: Lung Cellular and Molecular Physiology
State
WV
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