Virus-induced eosinophil mediator release requires antigen-presenting and CD4+ T cells - 15/08/11
Reprint requests: Darryl J. Adamko, MD, FRCP(C), Division of Pediatric Pulmonary Medicine, Pulmonary Research Group, Faculty of Medicine and Dentistry, 567B HMRC, University of Alberta, Edmonton, Alberta, Canada, T6G 2S2.Abstract |
Background |
The most frequent trigger of asthma exacerbation is infection with common airway viruses; however, the precise mechanism regulating such severe reactions is not understood. The presence of airway eosinophil products is a unique feature detected in asthmatic airways. Using an animal model, we previously demonstrated that T cells play an important role in regulating an eosinophil-dependant pathway of virus-induced airway hyperreactivity. We hypothesize that human eosinophils respond to viruses, although only after interaction with T cells.
Objectives |
We sought to determine whether eosinophils can respond to airway viruses in vitro and determine the mechanism of response.
Methods |
An in vitro coculture model of human eosinophils, antigen-presenting cells, and T cells was used with parainfluenza virus, respiratory syncytial virus, or rhinovirus. We measured release of eosinophil peroxidase (EPO) in concert with T-cell proliferation, cytokine release, and changes in T-cell phenotype.
Results |
The viruses induced release of EPO when coincubated in the presence of antigen-presenting cells (dendritic cells or macrophages) and T cells. Virus-mediated release was associated with proliferation of CD3+CD4+ T cells and release of cytokines. UV inactivation of the virus did not prevent virus-induced EPO release or T-cell proliferation. Proliferating CD4+ T cells show increased expression of CD25 and CD45RO. CD8+ T cells were not activated.
Conclusion |
Virus-induced EPO release can occur in the context of antigen presentation to CD4+ T cells.
Le texte complet de cet article est disponible en PDF.Key words : Eosinophil, virus infection, asthma exacerbation, eosinophil peroxidase, leukotriene, T cell, macrophage, dendritic cell
Abbreviations used : AHR, APC, Cys-LT, DC, EPO, LCMV, LT, PFU, PI3, PIV, RSV, RV
Plan
| Supported by the Sick Kids Foundation, the Canadian Institute for Health Research (CIHR), and the Alberta Heritage Foundation for Medical Research (AHFMR). D.J.A. is an Alberta Heritage Clinical Investigator, and R.M. is an Alberta Heritage Medical Scientist. |
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| Disclosure of potential conflict of interest: R. Moqbel has consulting arrangements with the Research Institute for Fragrance Materials, Inc, through an industrial partner, Toxcon Health Sciences Centre, Inc, and has received research support from Merck Frosst. D. J. Adamko has received research support from Merck Frosst, CV Technology, and Nycomed. The rest of the authors have declared that they have no conflict of interest. |
Vol 122 - N° 1
P. 69 - juillet 2008 Retour au numéro
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