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Am J Physiol Lung Cell Mol Physiol 279: L872-L877, 2000;
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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


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