Antigen-induced eosinophilic lung inflammation develops in mice deficient in chemokine eotaxin

被引:77
作者
Yang, Y [1 ]
Loy, J [1 ]
Ryseck, RP [1 ]
Carrasco, D [1 ]
Bravo, R [1 ]
机构
[1] Bristol Myers Squibb Pharmaceut Res Inst, Dept Oncol & Expt Pathol, Princeton, NJ 08543 USA
关键词
D O I
10.1182/blood.V92.10.3912.422k23_3912_3923
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 beta-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 beta-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. (C) 1998 by The American Society of Hematology.
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页码:3912 / 3923
页数:12
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