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*
Division of Basic Sciences, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206;
The Jackson Laboratory, Bar Harbor, ME 04609; and
Max-Planck-Institut für Immunbiologie, Freiburg, Germany
Viral respiratory infections can cause bronchial
hyperresponsiveness and exacerbate asthma. In mice, respiratory
syncytial virus (RSV) infection, which induces an immune response
dominated by IFN-
, results in airway hyperresponsiveness (AHR) and
eosinophil influx into the airways, both of which are prevented by
pretreatment with anti-IL-5 Ab. To delineate the role of IL-5,
IL-4, and IFN- in the development of RSV-induced AHR and lung
eosinophilia, we tested the ability of mice deficient in each of these
cytokines to develop these symptoms of RSV infection. Mice deficient in
either IL-5, IL-4, or IFN- were administered infectious RSV
intranasally, and 6 days later, airway responsiveness to inhaled
methacholine was assessed by barometric body plethysmography, and
numbers of lung eosinophils and production of IFN-, IL-4, and IL-5
by mononuclear cells from peribronchial lymph nodes were monitored. RSV
infection resulted in airway eosinophilia and AHR in both IL-4- and
IFN--deficient mice, but not in IL-5-deficient mice. Reconstitution
of IL-5-deficient mice with IL-5 restored these responses and enhanced
the responses in IL-4-deficient mice. Anti-VLA-4 (very late Ag-4)
treatment prevented lung eosinophilia and AHR following RSV infection
and IL-5 reconstitution. We conclude that in response to RSV, IL-5 is
essential for the influx of eosinophils into the lung and that
eosinophils in turn are critical for the development of AHR. IFN-
and IL-4 are not essential for these responses to RSV
infection.
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