Transgenic modeling of interleukin-13 in the lung.

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-beta(1), 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.

• Authors: Jack A Elias, Tao Zheng, Chun Geun Lee, Robert J Homer, Qingsheng Chen, Bing Ma, Michael Blackburn, Zhou Zhu
• Journal: Chest (Chest) Vol. 123 Issue 3 Suppl Pg. 339S-45S (Mar 2003) ISSN: 0012-3692 [Print] United States
• PMID: 12628967 (Publication Type: Journal Article, Review)

Chemical References

• Interleukin-13

Topics

• Animals
• Asthma (genetics, physiopathology)
• Disease Models, Animal
• Interleukin-13 (genetics, physiology)
• Lung (physiopathology)
• Mice
• Mice, Transgenic
• Transgenes (genetics, physiology)