Ablation of eosinophils leads to a reduction of allergen-induced pulmonary pathology

J. Paul Justice, Michael T. Borchers, Jeffrey R. Crosby, Edith M. Hines, Huahao H. Shen, Sergei I. Ochkur, Michael P. McGarry, Nancy A. Lee, James J. Lee

Research output: Contribution to journalArticlepeer-review

91 Scopus citations


A strategy to deplete eosinophils from the lungs of ovalbumin (OVA)-sensitized/challenged mice was developed using antibody-mediated depletion. Concurrent administration [viz. the peritoneal cavity (systemic) and as an aerosol to the lung (local)] of a rat anti-mouse CCR3 monoclonal antibody resulted in the abolition of eosinophils from the lung such that the airway lumen was essentially devoid of eosinophils. Moreover, perivascular/peribronchial eosinophil numbers were reduced to levels indistinguishable from saline-challenged animals. This antibody-mediated depletion was not accompanied by effects on any other leukocyte population, including, but not limited to, T cells and mast cells/basophils. In addition, no effects were observed on other underlying allergic inflammatory responses in OVA-treated mice, including OVA-specific immunoglobulin production as well as T cell-dependent elaboration of Th2 cytokines. The ablation of virtually all pulmonary eosinophils in OVA-treated mice (i.e., without concurrent effects on T cell activities) resulted in a significant decrease in mucus accumulation and abolished allergen-induced airway hyperresponsiveness. These data demonstrate a direct causative relationship between allergen-mediated pulmonary pathologies and eosinophils.

Original languageEnglish (US)
Pages (from-to)L169-L178
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 28-1
StatePublished - Jan 1 2003


  • Inflammation
  • Interleukin-5
  • Lung
  • Mouse
  • Transgenic/knockout

ASJC Scopus subject areas

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


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