ANTIINTERLEUKIN-5 ANTIBODY PREVENTS AIRWAY HYPERRESPONSIVENESS IN A MURINE MODEL OF AIRWAY SENSITIZATION

Eosinophils play a central role in the inflammatory response associate d with bronchial asthma. We studied the involvement of eosinophils in the development of airway hyperresponsiveness (AHR) in a mouse model o f allergic airway sensitization. Sensitization of BALB/c mice to OVA v ia the airways induced allergen-specific T-cell responses, IgE product ion, immediate cutaneous hypersensitivity (ICH), and increased airway reactivity. Airway sensitization was associated with eosinophil infilt ration of the airways and increased production of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells. Treatment of OVA-chall enged animals with anti-IL-5 antibody during the sensitization protoco l completely abolished the infiltration of eosinophils into the lung t issue and prevented the development of AHR without affecting levels of allergen-specific IgE, cutaneous hypersensitivity and allergen-specif ic T cell responses. These findings demonstrate that infiltration of l ung tissue by eosinophils, triggered by increased IL-5 production, is a major factor in the development of AHR in this mouse model of airway sensitization.