Transgenic modeling of interleukin-13 in the lung.
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.
Elias
Jack A
JA
Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8057, USA.
Zheng
Tao
T
Lee
Chun Geun
CG
Homer
Robert J
RJ
Chen
Qingsheng
Q
Ma
Bing
B
Blackburn
Michael
M
Zhu
Zhou
Z
D000818:Animals; D001249:Asthma / Q000235:genetics* / Q000503:physiopathology*; D004195:Disease Models, Animal; D018793:Interleukin-13 / Q000235:genetics* / Q000502:physiology*; D008168:Lung / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D019076:Transgenes / Q000235:genetics* / Q000502:physiology*
D018793:Interleukin-13