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Division of Basic Sciences, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206
In mice, respiratory syncytial virus (RSV) infection enhances
allergic airway sensitization, resulting in lung eosinophilia and in
airway hyperresponsiveness (AHR). The mechanisms by which RSV
contributes to development of asthma and its effects on allergic airway
sensitization in mice are not known. We tested whether these
consequences of RSV infection can be adoptively transferred by T cells
and whether depletion of T cell subsets prevents the effects of RSV
infection on subsequent airway sensitization. Mononuclear cells, T
lymphocytes, or CD4 or CD8 T cells from peribronchial lymph nodes
(PBLN) of RSV-infected mice were transferred into naive BALB/c mice
which were then exposed to OVA via the airways. Additionally,
RSV-infected mice were depleted of CD4 or CD8 T cells following acute
RSV infection but prior to airway sensitization. Following
sensitization, airway responsiveness to inhaled methacholine, numbers
of lung eosinophils, and levels of IFN-
, IL-4, and IL-5 in PBLN cell
cultures were monitored. Transfer of T cells from RSV-infected mice
resulted in increased eosinophil influx into the lungs, increased IL-5
production, and development of AHR following airway sensitization to
allergen. Transfer of CD8 but not CD4 T cells from the PBLN of
RSV-infected mice also resulted in AHR following 10 days of OVA
exposure. Further, depletion of CD8 T cells prevented these
consequences of RSV infection while CD4 T cell depletion reduced them.
We conclude that T cells, in particular CD8 T cells, are critical in
mediating RSV-induced development of lung eosinophilia and AHR
following allergic airway sensitization.
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