A murine model of allergic bronchopulmonary aspergillosis (ABPA), developed by exposure to Aspergillus fumigatus antigens, demonstrated eosinophilia of peripheral blood (PB), bone marrow (BM), and lung. The eosinophilia was abrogated by monoclonal anti-interleukin-5 (IL-5) antibody (TRFK-5) and not by an isotype control antibody (GL 113). Eosinophils in PB were enumerated from stained smears and their relative increase or decrease in cells from BM and lung was determined by an eosinophil peroxidase (EPO) assay (measured in optical density). Intraperitoneal injection of TRFK-5 in mice exposed to A. fumigatus antigen produced a significant reduction in eosinophils (PB 6.6 +/- 1.14% vs. 3.8 +/- 0.8%, P < .01) and EPO production in BM (0.935 +/- 0.03 vs. 0.615 +/- 0.02, P < .001). A similar reduction in EPO production in the lung (0.691 +/- 0.12 vs. 0.495 +/- 0.05, not significant) was also reflected in the histopathology for the different groups of mice. These findings confirming the role of IL-5 in eosinophilia, although not surprising, are significant in elucidating the immunopathogenesis of ABPA in the murine model. We conclude that in this model, eosinophilia may be due largely to the Th2 cytokine -IL-5 induced by A. fumigatus antigens.