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The Journal of Immunology, 2003, 170: 3296-3305.
Copyright © 2003 by The American Association of Immunologists

A Causative Relationship Exists Between Eosinophils and the Development of Allergic Pulmonary Pathologies in the Mouse1

HuaHao H. Shen*,{ddagger}, Sergei I. Ochkur{dagger}, Michael P. McGarry{dagger}, Jeffrey R. Crosby*, Edie M. Hines*, Michael T. Borchers{dagger}, Huiying Wang*,{ddagger}, Travis L. Biechelle*, Katie R. O’Neill*, Tracy L. Ansay*, Dana C. Colbert{dagger}, Stephania A. Cormier{dagger}, J. Paul Justice*, Nancy. A. Lee* and James J. Lee1,{dagger}

* Division of Hematology/Oncology, Department of Biochemistry and Molecular Biology, and {dagger} Division of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, S. C. Johnson Medical Research Center, Scottsdale, AZ 85259; and {ddagger} Department of Respiratory Medicine, Second Hospital, Zhejiang University College of Medicine, Hangzhou, China

Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5-/- mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5-/- mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5-/- mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5-/- mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4+ T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.




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