Abstract
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 α4-integrin signaling to the development of AHR in IL-5 transgenic mice through the administration of anti-CD49d (α4-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 α4-integrin signaling are necessary for the intrinsic AHR that develops in IL-5 transgenic mice.
Original language | English (US) |
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Pages (from-to) | L653-L659 |
Journal | American Journal of Physiology - Lung Cellular and Molecular Physiology |
Volume | 281 |
Issue number | 3 25-3 |
DOIs | |
State | Published - 2001 |
Keywords
- Cytokines
- Eosinophil
- Inflammation
- Interleukin-5
- T cell
ASJC Scopus subject areas
- Physiology
- Pulmonary and Respiratory Medicine
- Physiology (medical)
- Cell Biology