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Eosinophil Progenitors in Airway Diseases: Clinical Implications

Judah A. Denburg, MD; Paul K. Keith, MD, MSc
Author and Funding Information

*From the Division of Clinical Immunology and Allergy, McMaster University, Hamilton, ON, Canada.

Correspondence to: Judah A. Denburg, MD, HSC-3V46, McMaster University, 1200 Main St W, Hamilton, ON L8N 3Z5, Canada; e-mail: denburg@mcmaster.ca


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

Dr. Keith has received research support from Allergy Therapeutics, Nycomed, GSK, Merck, and Schering. He has served on advisory boards and received honoraria for lectures from Nycomed, AstraZeneca, GSK, Merck, and Schering.

Dr. Denburg has no financial or other potential conflicts of interest to disclose. Dr. Denburg holds grants from the Canadian Institutes for Health Research and AllerGen NCE Inc.


Chest. 2008;134(5):1037-1043. doi:10.1378/chest.08-0485
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Asthma, allergic rhinitis, nasal polyposis, chronic rhinosinusitis, and related forms of upper and lower airway diseases are often characterized by eosinophilic and basophilic inflammation, involving systemic processes. Eosinophil/basophil (Eo/B) lineage-committed progenitor cells in cord blood, peripheral blood, bone marrow, lung tissue, and sputum are up-regulated in the above conditions, and respond to allergen and other stimuli with increased differentiative and migratory capacity. A considerable body of evidence now exists showing that activation of such Eo/B-selective hemopoietic processes is not only associated with the onset and maintenance of allergic inflammation in atopic adults, but also with the development of the allergic diathesis. Moreover, eosinophilopoietic processes within hemopoietic compartments and, importantly, at mucosal tissue sites during an allergic inflammatory response provide novel targets for the treatment of allergy as a systemic process and disease.

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