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Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109
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 addresses the role of eotaxin/CCL11 during acute and chronic
allergic airway responses to the fungus Aspergillus
fumigatus. Mice lacking the eotaxin gene (Eo
/
) and wild-type
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. 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.
eosinophil; allergy; airway hyperreactivity
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