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Articles in PresS, published online ahead of print September 13, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00260.2002
Submitted on August 2, 2002
Accepted on September 12, 2002
1 Division of Hematology/Oncology, Mayo Clinic Scottsdale, Scottsdale, AZ, USA
2 Division of Pulmonary Medicine, Mayo Clinic Scottsdale, Scottsdale, AZ, USA
3 Department of Respiratory Medicine, Second Hospital, Zhejiang University College of Medicine, HangZhou, PR, China
* To whom correspondence should be addressed. E-mail: jjlee{at}mayo.edu.
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.
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