In humans, respiratory
viral infections lead to increased airway responsiveness and exacerbations of
asthma. In the present study, the role of
interleukin-5 (IL-5) in virus-induced
airway hyperresponsiveness and
inflammation was examined in guinea pigs. In animals treated with control antibody, parainfluenza-3 virus significantly potentiated (219%) the
histamine-induced increase in lung resistance compared with vehicle treatment. In addition,
viral infection significantly increased (130 to 450%) the responsiveness of isolated tracheal segments to
histamine in animals treated with control antibody. In guinea pigs treated with control antibody, the numbers of eosinophils (226%), neutrophils (1,380%), and monocytes (626%) in bronchoalveolar lavage fluid were significantly increased after
viral infection. The level of major basic
protein in bronchoalveolar lavage fluid was not altered after
viral infection. In addition, electron microscopic examination of eosinophils in airway tissue and alveolar lumen did not point to increased degranulation after
viral infection. In guinea pigs treated with antibody to
IL-5 the virus-induced
airway hyperresponsiveness to
histamine both in vivo and in vitro was almost completely inhibited. In guinea pigs treated with anti-IL-5,
viral infection significantly increased the numbers of eosinophils (234%), neutrophils (1,255%), and monocytes (617%) in bronchoalveolar lavage fluid. These data suggest that
IL-5 plays an important role in
airway hyperresponsiveness to
histamine but not in the infiltration of eosinophils after respiratory
viral infection.