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Defining a Link with Asthma in Mice Congenitally Deficient in Eosinophils
James J. Lee,1,2*Dawn Dimina,1,2MiMi P. Macias,1,2Sergei I. Ochkur,1,2Michael P. McGarry,1,2Katie R. O'Neill,2,3Cheryl Protheroe,2,3Ralph Pero,2,3Thanh Nguyen,1,2Stephania A. Cormier,1,2Elizabeth Lenkiewicz,1,2Dana Colbert,2,3Lisa Rinaldi,4Steven J. Ackerman,5Charles G. Irvin,4Nancy A. Lee2,3*
Eosinophils are often dominant inflammatory cells present inthe lungs of asthma patients. Nonetheless, the role of theseleukocytes remains poorly understood. We have created a transgenicline of mice (PHIL) that are specifically devoid of eosinophils,but otherwise have a full complement of hematopoietically derivedcells. Allergen challenge of PHIL mice demonstrated that eosinophilswere required for pulmonary mucus accumulation and the airwayhyperresponsiveness associated with asthma. The developmentof an eosinophil-less mouse now permits an unambiguous assessmentof a number of human diseases that have been linked to thisgranulocyte, including allergic diseases, parasite infections,and tumorigenesis.
1 Division of Pulmonary Medicine, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA. 2 Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA. 3 Division of Hematology/Oncology, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA. 4 Vermont Lung Center, Department of Medicine, University of Vermont, Burlington, VT 05405, USA. 5 Department of Biochemistry and Molecular Biology, University of Illinois, College of Medicine, Chicago, IL 60612, USA.
Present address: The EAR Foundation of Arizona, Phoenix, AZ85008, USA.
Present address: Department of Biology, Louisiana State University,Baton Rouge, LA 70803, USA.
* To whom correspondence should be addressed. E-mail: jjlee{at}mayo.edu (J.J.L.) and nlee{at}mayo.edu (N.A.L.)
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In Science Magazine
PERSPECTIVES
Marsha Wills-Karp and Christopher L. Karp (17 September 2004) Science305 (5691), 1726.
[DOI: 10.1126/science.1104134] |Summary »|Full Text »|PDF »
REPORTS
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[DOI: 10.1126/science.1100283] |Abstract »|Full Text »|PDF »|Supporting Online Material »
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P. C. Fulkerson, H. Zhu, D. A. Williams, N. Zimmermann, and M. E. Rothenberg (2005)
Blood
106, 436-443
|Abstract »|Full Text »|PDF »
Airway Hyperresponsiveness in the Absence of CD4+ T Cells after Primary but Not Secondary Challenge.
A. Joetham, K. Takeda, C. Taube, N. Miyahara, A. Kanehiro, A. Dakhama, and E. W. Gelfand (2005)
Am. J. Respir. Cell Mol. Biol.
33, 89-96
|Abstract »|Full Text »|PDF »
No audible wheezing: nuggets and conundrums from mouse asthma models.
Identification of a Cooperative Mechanism Involving Interleukin-13 and Eotaxin-2 in Experimental Allergic Lung Inflammation.
S. M. Pope, P. C. Fulkerson, C. Blanchard, H. S. Akei, N. M. Nikolaidis, N. Zimmermann, J. D. Molkentin, and M. E. Rothenberg (2005)
J. Biol. Chem.
280, 13952-13961
|Abstract »|Full Text »|PDF »
Activation of the Prostaglandin D2 Receptor DP2/CRTH2 Increases Allergic Inflammation in Mouse.
I. Spik, C. Brenuchon, V. Angeli, D. Staumont, S. Fleury, M. Capron, F. Trottein, and D. Dombrowicz (2005)
J. Immunol.
174, 3703-3708
|Abstract »|Full Text »|PDF »
Pharmacological Targeting of Anaphylatoxin Receptors during the Effector Phase of Allergic Asthma Suppresses Airway Hyperresponsiveness and Airway Inflammation.
R. Baelder, B. Fuchs, W. Bautsch, J. Zwirner, J. Kohl, H. G Hoymann, T. Glaab, V. Erpenbeck, N. Krug, and A. Braun (2005)
J. Immunol.
174, 783-789
|Abstract »|Full Text »|PDF »
The eosinophil in airway remodelling and hyperresponsiveness in asthma: participant or bystander?.
Present address: The EAR Foundation of Arizona, Phoenix, AZ 85008, USA. 
Present address: Department of Biology, Louisiana State University, Baton Rouge, LA 70803, USA. 
