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Morphometry Explains Variation in Airway Responsiveness in Transgenic Mice Overexpressing Interleukin-6 and Interleukin-11 in the Lung*

Charles Kuhn, MD; Robert J. Homer, MD, PhD; Zhou Zhu, MD, PhD; Nicholas Ward, MD; Jack A. Elias, MD
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*From the Department of Pathology (Dr. Kuhn), Brown University School of Medicine, Providence, RI; and the Departments of Pathology (Dr. Homer) and Pulmonary and Critical Care Medicine (Drs. Zhu, Ward, and Elias), Yale University, New Haven, CT.

Correspondence to: Charles Kuhn, MD, Pathology Department, Memorial Hospital of Rhode Island, Pawtucket, RI 02860



Chest. 2000;117(5_suppl_1):260S-262S. doi:10.1378/chest.117.5_suppl_1.260S
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Abbreviations: AA = alveolar wall attached; AHR = airway hyperreactivity; CC10 = Clara cell 10-kd protein; IL = interleukin; S/V = surface/volume ratio

The basis for airway hyperreactivity (AHR) accompanying COPD is poorly understood. Structural changes may play a role. We have generated transgenic mice that overexpress related cytokines, interleukin (IL)-6 and IL-11, in their airways, which were controlled by the Clara cell 10-kd protein (CC10) promoter. Despite some similar structural abnormalities, their airway physiology differed. CC10-IL-6 mice had normal expiratory flow and decreased reactivity to methacholine,1 while CC10-IL-11 mice had airflow obstruction and hyperreactivity.2 To clarify this difference, a morphometric study was undertaken of the lung parenchyma and bronchioles of the two transgenic strains and littermate controls.

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