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Am J Physiol Lung Cell Mol Physiol (February 8, 2002). doi:10.1152/ajplung.00341.2001
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Articles in PresS, published online ahead of print February 8, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00341.2001
Submitted on August 27, 2001
Accepted on February 5, 2002

Eotaxin/CCL11 is involved in acute, but not chronic, allergic airway responses to Aspergillus fumigatus

Jane M Schuh1, Kate Blease1, Steven L Kunkel1, and Cory M Hogaboam1*

1 Pathology, University of Michigan Medical School, Ann Arbor, MI, USA

* To whom correspondence should be addressed. E-mail: hogaboam{at}med.umich.edu.

Eotaxin/CCL11 is a major chemoattractant for eosinophils and Th2 cells. As such, it represents an attractive target in the treatment of allergic disease. The present study addressed the role of eotaxin/CCL11 during acute and chronic allergic airway responses to the fungus Aspergillus fumigatus. Mice lacking the eotaxin gene (Eo-/-) and wildtype mice (Eo+/+) were sensitized to A. fumigatus and received either an intratracheal challenge with soluble A. fumigatus antigens (acute model) or an intratracheal challenge with live A. fumigatus spores or conidia (chronic model). Airway hyperresponsiveness and eosinophil, but not T cell, recruitment were significantly decreased at 24 h after the soluble allergen in A. fumigatus-sensitized Eo-/- mice compared with similarly sensitized Eo+/+ mice. In contrast, the development of chronic allergic airway disease due to A. fumigatus conidia was not altered by the lack of eotaxin. Taken together, these data suggest that eotaxin initiates allergic airway disease due to A. fumigatus, but this chemokine did not appear to contribute to the maintenance of A. fumigatus-induced allergic airway disease.




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