| First Author | Borchers MT | Year | 2001 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 281 |
| Issue | 3 | Pages | L653-9 |
| PubMed ID | 11504693 | Mgi Jnum | J:132284 |
| Mgi Id | MGI:3775598 | Doi | 10.1152/ajplung.2001.281.3.L653 |
| Citation | Borchers MT, et al. (2001) Intrinsic AHR in IL-5 transgenic mice is dependent on CD4(+) cells and CD49d-mediated signaling. Am J Physiol Lung Cell Mol Physiol 281(3):L653-9 |
| abstractText | 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. |
