Transgenic modeling of interleukin-13 in the lung

Jack A. Elias, Tao Zheng, Chun Geun Lee, Robert J. Homer, Qingsheng Chen, Bing Ma, Michael Blackburn, Zhou Zhu

Research output: Contribution to journalArticlepeer-review

Abstract

Interleukin (IL)-13 is a key cytokine in asthma pathogenesis. We used constitutive and inducible overexpression transgenic mice to characterize the mechanisms by which IL-13 causes phenotypic alterations in the lung. These studies demonstrated that chemokine receptor-2, transforming growth factor-β1, and IL-11 play an important role in the regulation of inflammation and remodeling in the IL-13-treated lung. The study results also demonstrated that IL-13 induces vascular endothelial growth factor, which causes bronchial circulation neovascularization in the murine airway. Last, it was demonstrated that IL-13 induces adenosine accumulation and that adenosine in turn stimulates IL-13 elaboration. These approaches validated in vivo genetic targets against which therapies can be directed to selectively regulate aspects of the IL-13 phenotype.

Original languageEnglish (US)
Pages (from-to)339S-345S
JournalCHEST
Volume123
Issue number3 SUPPL.
DOIs
StatePublished - Mar 1 2003

Keywords

  • Adenosine
  • Airway remodeling
  • Interleukin-11
  • Interleukin-13
  • Transforming growth factor-β
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

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