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Published ahead of print on June 2, 2009, doi:10.1165/rcmb.2009-0122RC

Am. J. Respir. Cell Mol. Biol., Volume 41, Number 4, October 2009, 379-384

A more recent version of this article appeared on October 1, 2009
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Submitted on April 8, 2009
Accepted on May 28, 2009

Macrophage Chitinase 1 Stratifies Chronic Obstructive Lung Disease

Eugene Agapov1, John T. Battaile1, Rose Tidwell1, Ramsey Hachem1, G. Alexander Patterson2, Richard A. Pierce1, Jeffrey J. Atkinson1, and Michael J. Holtzman3*

1 Medicine, Washington University School of Medicine, St. Louis, Missouri, United States, 2 Surgery, Washington University School of Medicine, St. Louis, Missouri, United States, 3 Medicine, Washington University School of Medicine, St. Louis, Missouri, United States; Cell Biology, Washington University School of Medicine, St. Louis, Missouri, United States

* To whom correspondence should be addressed. E-mail: holtzmanm{at}wustl.edu.

Diagnosis and therapy of chronic inflammatory lung disease is limited by the need for individualized biomarkers that provide insight into pathogenesis. Herein we show that mouse models of chronic obstructive lung disease exhibit an increase in lung chitinase production but cannot predict which chitinase family member may be equivalently increased in humans with corresponding lung disease. Moreover, we demonstrate that lung macrophage production of chitinase 1 is selectively increased in a subset of subjects with severe chronic obstructive pulmonary disease (COPD), and this increase is reflected in plasma levels. The findings provide a means to noninvasively track alternatively activated macrophages in chronic lung disease and thereby better differentiate molecular phenotypes in heterogeneous patient populations.




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Am. J. Respir. Cell Mol. Biol., October 1, 2009; 41(4): 377 - 378.
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