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Am J Physiol Lung Cell Mol Physiol 284: L169-L178, 2003. First published September 13, 2002; doi:10.1152/ajplung.00260.2002
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Vol. 284, Issue 1, L169-L178, January 2003

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

J. Paul Justice1, Michael T. Borchers2, Jeffrey R. Crosby1, Edith M. Hines1, Huahao H. Shen1,3, Sergei I. Ochkur2, Michael P. McGarry2, Nancy A. Lee1, and James J. Lee2

1 Division of Hematology/Oncology and 2 Pulmonary Medicine, Department of Biochemistry and Molecular Biology, S. C. Johnson Medical Research Building, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259; and 3 Department of Respiratory Medicine, Second Hospital, Zhejiang University College of Medicine, HangZhou 310009, People's Republic of China

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.

mouse; lung; inflammation; transgenic/knockout; interleukin-5


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