ANTIBODY TO INTERLEUKIN-5 INHIBITS VIRUS-INDUCED AIRWAY HYPERRESPONSIVENESS TO HISTAMINE IN GUINEA-PIGS

In humans, respiratory viral infections lead to increased airway respo nsiveness and exacerbations of asthma. In the present study, the role of interleukin-5 (IL-5) in virus-induced airway hyperresponsiveness an d inflammation was examined in guinea pigs. In animals treated with co ntrol antibody, parainfluenza-3 virus significantly potentiated (219%) the histamine-induced increase in lung resistance compared with vehic le treatment. In addition, viral infection significantly increased (13 0 to 450%) the responsiveness of isolated tracheal segments to histami ne in animals treated with control antibody. In guinea pigs treated wi th control antibody, the numbers of eosinophils (226%), neutrophils (1 ,380%), and monocytes (626%) in bronchoalveolar lavage fluid were sign ificantly increased after viral infection. The level of major basic pr otein in bronchoalveolar lavage fluid was not altered after viral infe ction. In addition, electron microscopic examination of eosinophils in airway tissue and alveolar lumen did not point to increased degranula tion af ter viral infection. In guinea pigs treated with antibody to I L-5 the virus-induced airway hyperresponsiveness to histamine both in vivo and in vitro was almost completely inhibited. In guinea pigs trea ted with anti-IL-5, viral infection significantly increased the number s of eosinophils(234%), neutrophils (1,255%), and monocytes (617%) in bronchoalveolar lavage fluid. These data suggest that IL-5 plays an im portant role in airway hyperresponsiveness to histamine but not in the infiltration of eosinophils after respiratory viral infection.