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

E. Hamelmann, A. Oshiba, J. Loader, C. L. Larsen, C. Gleich, J. Lee, E. W. Gelfand

Research output: Contribution to journalArticlepeer-review

243 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)819-825
Number of pages7
JournalAmerican journal of respiratory and critical care medicine
Volume155
Issue number3
DOIs
StatePublished - 1997

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Fingerprint Dive into the research topics of 'Antiinterleukin-5 antibody prevents airway hyperresponsiveness in a murine model airway sensitization'. Together they form a unique fingerprint.

Cite this