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Transgenic Modeling of Interleukin-13 in the Lung*

Jack A. Elias, MD; Tao Zheng, MD; Chun Geun Lee, MD, PhD; Robert J. Homer, MD, PhD; Qingsheng Chen, MD; Bing Ma, PhD; Michael Blackburn, PhD; Zhou Zhu, MD, PhD
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*From the Departments of Internal Medicine (Drs. Elias, Zheng, Lee, Chen, Ma, and Zhu), Section of Pulmonary and Critical Care Medicine, and Pathology (Dr. Homer), Yale University School of Medicine, New Haven, CT; and the Department of Biochemistry and Molecular Biology (Dr. Blackburn), University of Texas Health Science Center, Houston Medical School, Houston, TX 77030.

Correspondence to: Jack A. Elias, MD, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, Department of Internal Medicine, 333 Cedar St, LCI 105, New Haven, CT 06520-8057.



Chest. 2003;123(3_suppl):339S-345S. doi:10.1378/chest.123.3_suppl.339S
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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.

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