Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleutkin-5 but not immunoglobulin E or B lymphocytes

We previously defined a role for B cells and allergen-specific immunoglobul ins in the development of allergic sensitization, airway inflammation, and airway hyperresponsiveness (AHR), using a 10-d protocol in which allergen e xposure occurred exclusively via the airways, without adjuvant. In the pres ent protocol, normal and B-cell-deficient (mu Mt(-/-)) mice were sensitized intraperitoneally to ovalbumin (OVA) and challenged with OVA via the airwa ys in order to examine the requirements for AHR with this protocol. T-cell activation (antigen-specific proliferative responses and Th2-type cytokine production) and eosinophil infiltration in the peribronchial regions of the airways, with signs of eosinophil activation and degranulation, occurred i n both experimental groups. In contrast to the 10-d protocol, increased in vivo airway responsiveness to methacholine and in vitro tracheal smooth-mus cle responses to electrical field stimulation were observed in both normal and B-cell-deficient mice, and these responses were inhibited by anti-inter leukin (IL)-5 administration before airway challenge. These data show that IL-5, but not B cells or allergen-specific IgE, are required for eosinophil airway infiltration and the development of AHR following allergen/alum sen sitization and repeated airway challenge with allergen. These results empha size that the use of different sensitization and challenge protocols can in fluence the requirements for development of AHR.