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 language | English (US) |
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Pages (from-to) | 339S-345S |
Journal | CHEST |
Volume | 123 |
Issue number | 3 SUPPL. |
DOIs | |
State | Published - 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