Anti-interleukin 5 but not Anti-IgE prevents airway inflammation and airway hyperresponsiveness

The role of IL-5 and allergen-specific IgE in the development of eosinophil ic airway inflammation and airway hyperresponsiveness (AHR) was investigate d in a murine model. BALB/c mice were sensitized to ovalbumin (OVA) by intr aperitoneal injection on Days 1 and 14, followed by airway challenge with O VA on Days 28 and 29. Anti-IL-5 (TRFK-5) or anti-IgE (antibody 1-5) was adm inistered before each airway challenge. Sensitized and challenged mice deve loped increased OVA-specific IgE serum levels, Th2 cytokine production by p eribronchial lymph node (PBLN) cells, increased numbers of eosinophils (pre dominantly located in the peribronchial regions of the lungs), and increase d airway responsiveness to methacholine (MCh). Anti-IgE treatment significa ntly decreased serum anti-OVA IgE levels and prevented the development of a naphylaxis but failed to affect T cell function, eosinophil airway infiltra tion, and AHR in sensitized and challenged mice. In contrast, treatment wit h anti-IL-5 antibody did not affect B cell (Ig serum levels), i cell (cytok ine production), or mast cell function (immediate cutaneous reactivity) but completely inhibited development of eosinophilic lung inflammation and AHR . These data identify IL-5-mediated eosinophilia as a major target for deve lopment of AHR in this model, with little effect resulting from neutralizat ion of IgE.