The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/2/785/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 4, February 17, 1997 785-790

Brief Definitive Reports

Targeted Disruption of the Chemokine Eotaxin Partially Reduces Antigen-induced Tissue Eosinophilia

Marc E. Rothenberg*, James A. MacLean{ddagger}, Eric Pearlman||, Andrew D. Luster§, and Philip Leder*

From the * Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; {ddagger} Allergy Unit, § Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; || Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106

The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and have recently been shown to inhibit human immunodeficiency virus entry into cells. Eotaxin is a C–C chemokine implicated in the recruitment of eosinophils in a variety of inflammatory disorders and, unlike all other eosinophil chemoattractants, is eosinophil specific. However, given the large number of chemoattractants that have activities on eosinophils, it is unclear whether eotaxin has an important role in vivo. Furthermore, it remains unclear why there is constitutive expression of eotaxin in healthy states in the absence of eosinophilic inflammation. To begin to determine the significance of eotaxin at baseline and during eosinophil-mediated disease processes, we have used targeted gene disruption to generate mice that are deficient in eotaxin. Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis. Surprisingly, a role for eotaxin in regulating the constitutive number of eosinophils in the peripheral circulation is also demonstrated. These results indicate a contributory role for eotaxin in the generation of peripheral blood and antigen-induced tissue eosinophilia.

Address correspondence to Marc Rothenberg, Department of Pediatrics, 3333 Burnet Avenue, Cincinnati, OH 45229.


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