Gq signaling is required for allergen-induced pulmonary eosinophilia

被引:17
作者
Borchers, MT
Justice, PJ
Ansay, T
Mancino, V
McGarry, MP
Crosby, J
Simon, MI
Lee, NA
Lee, JJ
机构
[1] Mayo Clin Scottsdale, Div Pulm Med, Dept Biochem & Mol Biol, Scottsdale, AZ 85259 USA
[2] Mayo Clin Scottsdale, Div Hematol & Oncol, Scottsdale, AZ 85259 USA
[3] CALTECH, Div Biol, Pasadena, CA 91125 USA
关键词
D O I
10.4049/jimmunol.168.7.3543
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The complexity and magnitude of interactions leading to the selective infiltration of eosinophils in response to inhaled allergens are formidable obstacles to a larger understanding of the pulmonary pathology associated with allergic asthma. This study uses knockout mice to demonstrate a novel function for the heterotrimeric G protein, G(q), in the regulation of pulmonary eosinophil recruitment. In the absence of G(q) signaling, eosinophils failed to accumulate in the lungs following allergen challenge. These studies demonstrate that the inhibition of eosinophil accumulation in the airways is attributed to the failure of hemopoietically derived cells to elaborate GM-CSF in the airways. The data suggest that activation of a G(q)-coupled receptor(s) on resident leukocytes in the lung elicits expression of GM-CSF, which, in turn, is required for allergen-induced pulmonary eosinophilia, identifying a novel pathway of cosinophil-associated effector functions leading to pulmonary pathology in diseases such as asthma.
引用
收藏
页码:3543 / 3549
页数:7
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