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Interleukin-13 Induces Surfactant Function Abnormality in the Murine Lung*

Zhou Zhu, MD, PhD; Goran Enhorning, MD, PhD; Tao Zheng, MD; Qingsheng Chen, MD; Ning Yuan Chen, BS; Robert Homer, MD, PhD; Jack A. Elias, MD
Author and Funding Information

*From the Departments of Internal Medicine (Drs. Zhu, Zheng, Q. Chen, and Elias and Ms N-Y Chen) and Pathology (Dr. Homer), Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT; and the Department of Obstetrics/Gynecology (Dr. Enhorning), State University of New York at Buffalo, Buffalo, NY.

Correspondence to: Zhou Zhu, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 333 Cedar St, New Haven, CT 06520; e-mail: zhou.zhu@yale.edu



Chest. 2003;123(3_suppl):375S-376S. doi:10.1378/chest.123.3_suppl.375S
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Overexpression of interleukin (IL)-13 in the murine lung causes eosinophil-predominant and macrophage-predominant inflammation, increased airway resistance, and airway hyperresponsiveness.1 These mice also manifest increased production and accumulation of surfactant apoproteins and alterations in surfactant phospholipid composition.2 However, the effects of IL-13 on surfactant function have not been defined. We hypothesized that IL-13 alters surfactant function as well as production.

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