Antiinterleukin-5 antibody prevents airway hyperresponsiveness in a murine model of airway sensitization

Am J Respir Crit Care Med. 1997 Mar;155(3):819-25. doi: 10.1164/ajrccm.155.3.9117011.


Eosinophils play a central role in the inflammatory response associated with bronchial asthma. We studied the involvement of eosinophils in the development of airway hyperresponsiveness (AHR) in a mouse model of allergic airway sensitization. Sensitization of BALB/c mice to OVA via the airways induced allergen-specific T-cell responses, IgE production, immediate cutaneous hypersensitivity (ICH), and increased airway reactivity. Airway sensitization was associated with eosinophil infiltration of the airways and increased production of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells. Treatment of OVA-challenged animals with anti-IL-5 antibody during the sensitization protocol completely abolished the infiltration of eosinophils into the lung tissue and prevented the development of AHR without affecting levels of allergen-specific IgE, cutaneous hypersensitivity and allergen-specific T cell responses. These findings demonstrate that infiltration of lung 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cells, Cultured
  • Disease Models, Animal
  • Eosinophils / immunology*
  • Female
  • Immunization
  • Interleukin-4 / immunology*
  • Interleukin-5 / immunology*
  • Leukocyte Count
  • Lung / immunology
  • Lung / pathology
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / immunology
  • Respiratory Hypersensitivity / immunology*


  • Interleukin-5
  • Interleukin-4
  • Ovalbumin