AJP - Lung AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 279: L872-L877, 2000;
1040-0605/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dokka, S.
Right arrow Articles by Rojanasakul, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dokka, S.
Right arrow Articles by Rojanasakul, Y.
Vol. 279, Issue 5, L872-L877, November 2000

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

Sujatha Dokka1, Carl J. Malanga1, Xianglin Shi2, Fei Chen2, Vincent Castranova2, and Yon Rojanasakul1

1 Department of Pharmaceutical Sciences, West Virginia University Health Sciences Center, Morgantown 26506; and 2 Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505

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.

tumor necrosis factor-alpha ; gene transfer; liposome


This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. Garantziotis, D. M. Brass, J. Savov, J. W. Hollingsworth, E. McElvania-TeKippe, K. Berman, J. K. L. Walker, and D. A. Schwartz
Leukocyte-Derived IL-10 Reduces Subepithelial Fibrosis Associated with Chronically Inhaled Endotoxin
Am. J. Respir. Cell Mol. Biol., December 1, 2006; 35(6): 662 - 667.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
V. Deleuze, J. Lefort, M. F. Bureau, D. Scherman, and B. B. Vargaftig
LPS-induced bronchial hyperreactivity: interference by mIL-10 differs according to site of delivery
Am J Physiol Lung Cell Mol Physiol, January 1, 2004; 286(1): L98 - L105.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Ye, L. Wang, X. Zhang, V. Tantishaiyakul, and Y. Rojanasakul
Inhibition of TNF-alpha gene expression and bioactivity by site-specific transcription factor-binding oligonucleotides
Am J Physiol Lung Cell Mol Physiol, February 1, 2003; 284(2): L386 - L394.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
D. A. Knight, P. G. Holt, and P. D. Sly
Lipopolysaccharide Inhibits the Late-Phase Response to Allergen by Altering Nitric Oxide Synthase Activity and Interleukin-10
Am. J. Respir. Cell Mol. Biol., May 1, 2001; 24(5): 640 - 646.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online