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Division of Basic Sciences, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206
Viral respiratory infections can cause bronchial
hyperresponsiveness and exacerbate asthma. In mice, respiratory
syncytial virus (RSV) infection results in airway hyperresponsiveness
(AHR) and eosinophil influx into the airways. The immune cell
requirements for these responses to RSV infection are not well defined.
To delineate the role of CD8 T cells in the development of RSV-induced
AHR and lung eosinophilia, we tested the ability of mice depleted of
CD8 T cells to develop these symptoms of RSV infection. BALB/c mice
were depleted of CD8 T cells using anti-CD8 Ab treatment before
intranasal administration of infectious RSV. Six days postinfection,
airway responsiveness to inhaled methacholine was assessed by
barometric body plethysmography, and numbers of lung eosinophils and
levels of IFN-
, IL-4, and IL-5 in bronchoalveolar lavage fluid were
monitored. RSV infection resulted in airway eosinophilia and AHR in
control mice, but not in CD8-depleted animals. Further, whereas
RSV-infected mice secreted increased amounts of IL-5 into the airways
as compared with noninfected controls, no IL-5 was detectable in both
bronchoalveolar lavage fluid and culture supernatants from CD8-depleted
animals. Treatment of CD8-depleted mice with IL-5 fully restored both
lung eosinophilia and AHR. We conclude that CD8 T cells are essential
for the influx of eosinophils into the lung and the development of AHR
in response to RSV infection.
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