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Science 26 September 1997:
Vol. 277. no. 5334, pp. 2002 - 2004
DOI: 10.1126/science.277.5334.2002

Reports

Requirement for Macrophage Elastase for Cigarette Smoke-Induced Emphysema in Mice

R. Dean Hautamaki, Dale K. Kobayashi, Robert M. Senior, Steven D. Shapiro *

To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.

Departments of Internal Medicine, and Cell Biology and Physiology, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO 63110, USA.
*   To whom correspondence should be addressed. E-mail: sshapiro{at}imgate.wustl.edu


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NADPH Oxidase Restrains the Matrix Metalloproteinase Activity of Macrophages.
S. Y. Kassim, X. Fu, W. C. Liles, S. D. Shapiro, W. C. Parks, and J. W. Heinecke (2005)
J. Biol. Chem. 280, 30201-30205
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Time course of cigarette smoke-induced pulmonary inflammation in mice.
A. I. D'hulst, K. Y. Vermaelen, G. G. Brusselle, G. F. Joos, and R. A. Pauwels (2005)
Eur. Respir. J. 26, 204-213
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Short-Term Cigarette Smoke Exposure Enhances Allergic Airway Inflammation in Mice.
K. B. Moerloose, R. A. Pauwels, and G. F. Joos (2005)
Am. J. Respir. Crit. Care Med. 172, 168-172
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Overexpression of Stat3C in Pulmonary Epithelium Protects against Hyperoxic Lung Injury.
X. Lian, Y. Qin, S. A. Hossain, L. Yang, A. White, H. Xu, J. M. Shipley, T. Li, R. M. Senior, H. Du, et al. (2005)
J. Immunol. 174, 7250-7256