Transient contribution of mast cells to pulmonary eosinophilia but not to hyper-responsiveness
Article first published online: 28 FEB 2002
Clinical & Experimental Allergy
Volume 32, Issue 1, pages 140–148, January 2002
How to Cite
Ogawa, K., Kaminuma, O., Kikkawa, H., Nakata, A., Asahina, M., Egan, R. W., Akiyama, K. and Mori, A. (2002), Transient contribution of mast cells to pulmonary eosinophilia but not to hyper-responsiveness. Clinical & Experimental Allergy, 32: 140–148. doi: 10.1046/j.0022-0477.2001.01248.x
- Issue published online: 28 FEB 2002
- Article first published online: 28 FEB 2002
- Submitted 19 October 2000; revised 25 January 2001; accepted 30 June 2001
- mast cell;
- eosinophilic inflammation;
- bronchial hyper-responsiveness;
- CD4+ T cell;
- cyclosporin A
Background We have recently demonstrated that the transfer of interleukin (IL)-5-producing CD4+ T cell clones into unprimed mice is sufficient for the development of eosinophilic inflammation in the bronchial mucosa upon antigen inhalation.
Objective The aim of this study was to elucidate the possible contribution of mast cells in eosinophilic inflammation and bronchial hyper-responsiveness (BHR), and to discriminate between the roles of CD4+ T cells and mast cells.
Methods Mast cell-deficient mice (WBB6F1-W/Wv) and their congenic normal littermates (WBB6F1−+/+) were immunized with ovalbumin and challenged by inhalation with the relevant antigen.
Results Airway eosinophilia was induced with equivalent intensity in +/+ and W/Wv mice 6, 24, 96 and 216 h after antigen inhalation. In contrast, 48 h after antigen challenge, eosinophilic infiltration into the bronchial mucosa was significantly less pronounced in W/Wv mice than in +/+ mice. Anti-CD4 monoclonal antibody (mAb), anti-IL-5 mAb, and cyclosporin A were administered next, demonstrating that the airway eosinophilia of W/Wv mice induced 48 h after antigen challenge was almost completely inhibited by each of these three treatments, but that of +/+ mice was significantly less susceptible. Bronchial responsiveness to acetylcholine was increased 48 h after antigen challenge and was not significantly different between +/+ and W/Wv mice. Administration of anti-IL-5 mAb completely inhibited the development of BHR in both +/+ and W/Wv mice.
Conclusion These results indicate that, in mice, mast cells do have a supplemental role in the development of pulmonary eosinophilia but not BHR. CD4+ T cells totally regulate these responses by producing IL-5.