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Published ahead of print on February 10, 2006, doi:10.1165/rcmb.2005-0314OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 34, pp. 711-718, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2005-0314OC

Multistrain Genetic Comparisons Reveal CCR5 as a Receptor Involved in Airway Hyperresponsiveness

Julia K. L. Walker, Adriana Ahumada, Bryan Frank, Renee Gaspard, Katherine Berman, John Quackenbush and David A. Schwartz

Department of Pulmonary, Allergy and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina; the Institute for Genomic Research, Rockville, Maryland; Dana-Farber Cancer Institute and the Harvard School of Public Health, Boston, Massachusetts; National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina

Correspondence and requests for reprints should be addressed to Julia K. L. Walker, Department of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27710. E-mail: walke082{at}mc.duke.edu

Asthma is a ubiquitous disease with a broad range of clinical phenotypes. To better understand the complex genetic and environmental interactions underlying asthma, we compared the gene–gene interactions of four genetically distinct mouse strains that demonstrate biologically distinct responses to allergen. Using DNA microarrays and knock-out mouse studies, we showed that CCR5 plays a definitive role in the development of ovalbumin-induced allergic airway inflammatory disease. In addition, gene expression profiling data have revealed other potential novel targets for therapeutics-based research and has enhanced the understanding of the molecular mechanisms underlying the etiology of "asthma."

Key Words: airway hyperresponsiveness • asthma • CCR5 • microarray • multistrain




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Copyright © 2006 American Thoracic Society.