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

Sujatha Dokka, Carl J. Malanga, Xianglin Shi, Fei Chen, Vincent Castranova, Yon Rojanasakul

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Interleukin (IL)-10 is an anti-infammatory 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)-α 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.

Original languageEnglish
Pages (from-to)L872-L877
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number5 23-5
StatePublished - 2000


  • Gene transfer
  • Liposome
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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