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Am J Physiol Lung Cell Mol Physiol 281: L653-L659, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 3, L653-L659, September 2001

Intrinsic AHR in IL-5 transgenic mice is dependent on CD4+ cells and CD49d-mediated signaling

Michael T. Borchers, J. Crosby, P. Justice, S. Farmer, E. Hines, J. J. Lee, and N. A. Lee

Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259

Overexpression of interleukin (IL)-5 by the airway epithelium in mice using the rat CC10 promoter (NJ.1726 line) leads to several histopathologies characteristic of human asthma, including airway hyperreactivity (AHR). We investigated the contribution of B and T cells, as well as CD4 expression, to the development of AHR in IL-5 transgenic mice. NJ.1726 mice on a T cell or CD4 knockout background, but not on a B cell knockout background, lost intrinsic AHR. These effects occurred without decreases in IL-5 or eosinophils. We further investigated the contribution of alpha 4-integrin signaling to the development of AHR in IL-5 transgenic mice through the administration of anti-CD49d (alpha 4-integrin) antibody (PS/2). Administration of PS/2 resulted in immediate (16-h) inhibition of AHR. The inhibition of AHR was not associated with a decrease in airway eosinophils. These studies demonstrate that, despite the presence of increased levels of IL-5 and eosinophils in the lungs of NJ.1726 mice, CD4+ cells and alpha 4-integrin signaling are necessary for the intrinsic AHR that develops in IL-5 transgenic mice.

cytokines; inflammation; eosinophil; T cell; interleukin-5


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