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Blood, Vol. 92 No. 10 (November 15), 1998:
pp. 3912-3923
Antigen-Induced Eosinophilic Lung Inflammation Develops in Mice
Deficient in Chemokine Eotaxin
Yi Yang,
James Loy,
Rolf-Peter Ryseck,
Daniel Carrasco, and
Rodrigo Bravo
From the Department of Oncology and Experimental Pathology,
Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton,
NJ.
The mechanisms that regulate the selective infiltration of
eosinophils in certain allergic diseases are still poorly understood. The CC chemokine eotaxin is a potent chemoattractant, highly specific for eosinophils. Recent studies have implicated that eotaxin plays an
important role in the recruitment of eosinophils in different inflammation processes. A number of other chemokines, cytokines, and
chemoattractants also have chemotactic activities for eosinophils and
some of them present high selectivity for eosinophils. To further study
the role of eotaxin in inflammation, we generated mutant mice with the
eotaxin gene disrupted and replaced by the Escherichia coli
 -galactosidase gene. These mice developed normally and had no
histologic or hematopoietic abnormalities. Furthermore, our studies
showed that the lack of eotaxin did not affect the recruitment of
eosinophils in the inflammation models induced by Sephadex beads and
thioglycollate, as well as in an experimental lung eosinophilia model
induced by ovalbumin aerosol challenge, even at the onset of the
inflammatory response. The replacement of the eotaxin gene by the
-galactosidase gene provided a useful marker to monitor the activity
of the eotaxin promoter under normal conditions and after antigen
challenges. Immunohistochemical staining suggested that endothelial
cells were the major sources of eotaxin expression.
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