Published online May 19, 2008
doi:10.1084/jem.20071836
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Walsh et al.
Strain-specific requirement for eosinophils in the recruitment of T cells to the lung during the development of allergic asthma
Elizabeth Rose Walsh1,2,
Nisebita Sahu1,3,
Jennifer Kearley4,
Ebony Benjamin4,
Boo Hyon Kang5,
Alison Humbles4, and
Avery August1
1 Center for Molecular Immunology and Infectious Disease and Department of Veterinary and Biomedical Sciences, 2 Pathobiology Graduate Program, 3 Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA 16802
4 Respiratory, Inflammation and Autoimmunity, Medimmune, Inc., Gaithersburg, MD 20878
5 Non-clinical Pathology Research Center, Medvill Co., Seoul, South Korea
CORRESPONDENCE Avery August: axa45{at}psu.edu
Eosinophils have been implicated as playing a major role in allergic airway responses. However, the importance of these cells to the development of this disease has remained ambiguous despite many studies, partly because of lack of appropriate model systems. In this study, using transgenic murine models, we more clearly delineate a role for eosinophils in asthma. We report that, in contrast to results obtained on a BALB/c background, eosinophil-deficient C57BL/6 
dblGATA mice (eosinophil-null mice via the DblGATA1 mutation) have reduced airway hyperresponsiveness, and cytokine production of interleukin (IL)-4, -5, and -13 in ovalbumin-induced allergic airway inflammation. This was caused by reduced T cell recruitment into the lung, as these mouse lungs had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2. Transferring eosinophils into these eosinophil-deficient mice and, more importantly, delivery of CCL11/eotaxin-1 into the lung during the development of this disease rescued lung T cell infiltration and airway inflammation when delivered together with allergen. These studies indicate that on the C57BL/6 background, eosinophils are integral to the development of airway allergic responses by modulating chemokine and/or cytokine production in the lung, leading to T cell recruitment.
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