Interleukin-4 receptor blockade prevents airway responses induced by antigen challenge in mice

Stephen H. Gavett, Daniel J. O'Hearn, Christopher L. Karp, Elizabeth A. Patel, Brian H. Schofield, Fred D. Finkelman, Marsha Wills-Karp

Research output: Contribution to journalArticlepeer-review

201 Scopus citations


The functional role of interleukin (IL)-4 in the development of airway hyperresponsiveness (AHR) and pulmonary eosinophilia in response to sensitization and challenge of mice with sheep red blood cells (SRBC) was examined. Control- and SRBC-sensitized A/J mice were treated with an antibody to the murine IL-4 receptor (anti-IL-4R) 3 days before intratracheal challenge with the antigen or vehicle only. Blockade of IL-4R significantly reduced antigen-induced AHR and prevented increases in goblet cells and bronchoalveolar lavage (BAL) eosinophils. Treatment with anti-IL-4R did not affect antigen-induced increases in lung mRNA and BAL protein levels of IL-5 and interferon-γ or IL-4 mRNA but did significantly increase IL-4 protein levels. Antigen-induced AHR was not reduced by treatment with antibodies to the adhesion molecules, vascular cell adhesion molecule-1 and very late activation antigen-4. Administration of IL-4 over a 7-day period did not increase airway reactivity or induce any changes in BAL cell numbers in naive mice. These results demonstrate that IL-4 is necessary for in vivo development of antigen-induced AHR, goblet cell metaplasia, and pulmonary eosinophilia.

Original languageEnglish (US)
Pages (from-to)L253-L261
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number2 16-2
StatePublished - Feb 1997


  • allergy
  • cytokine
  • goblet cell metaplasia

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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