ANTIBODY AGAINST INTERLEUKIN-5 PREVENTS ANTIGEN-INDUCED EOSINOPHIL INFILTRATION AND BRONCHIAL HYPERREACTIVITY IN THE GUINEA-PIG AIRWAYS

Interleukin-5 (IL-5) induces proliferation, differentiation and activa tion of eosinophils. An animal model of local allergen (airways) sensi tization was employed to study the effects of anti-IL-5 monoclonal ant ibody (mAb) on infiltration of eosinophils into inflammatory region, t he development of antigen-induced late asthmatic response (LAR) and th e increased bronchial responsiveness following LAR. Guinea pigs expose d to aerosolized ovalbumin (OVA) daily for 10 days developed an increa se in the number of eosinophils in the tracheal wall 24 h after aeroso lized OVA challenge. Furthermore, all animals developed an apparent LA R determined by the response with a 2-fold increase in respiratory res istance and showed an increase in bronchial responsiveness to acetylch oline 24 h after OVA challenge. In animals treated with anti-IL-5 mAb, however, eosinophil number in the tracheal wall dramatically decrease d compared with animals treated with control antibody. The development of LAR was also remarkably suppressed by anti-IL-5 mAb treatment, alt hough a similar magnitude of immediate bronchoconstriction was observe d. Moreover, in anti-IL-5 antibody-treated guinea pigs, an increase in bronchial responsiveness to acetylcholine significantly decreased. Da ta demonstrate that IL-5 is involved in airway eosinophilia, developme nt of LAR and an increase in bronchial responsiveness induced by aller gen sensitization via the airways. Development of IL-5 synthesis