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The Combination of Elastase and Sulfur Dioxide Exposure Causes COPD-Like Lesions in the Rat*

Urmila P. Kodavanti, PhD; Mette C. Jackson, BS; Allen D. Ledbetter, BS; Barry C. Starcher, PhD; Paul A. Evansky, BS; Adrian Harewood, BS; Darrell W. Winsett, BS; Daniel L. Costa, ScD
Author and Funding Information

*From the Pulmonary Toxicology Branch, Experimental Toxicology Division (Dr. Kodavanti, Ms. Jackson, Mr. Ledbetter, Mr. Evansky, Dr. Costa, and Mr. Winsett), National Health and Environment Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, NC; University of Texas Health Center (Dr. Starcher), Tyler, TX; and North Carolina Central University (Mr. Harewood), Durham, NC.

Correspondence to: Urmila Kodavanti, Research Biologist, MD-82, PTB/ETD/NHEERL, USEPA, Research Triangle Park, NC 27711



Chest. 2000;117(5_suppl_1):299S-302S. doi:10.1378/chest.117.5_suppl_1.299S
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Abbreviations: BALF = BAL fluid; LDH = lactate dehydrogenase; PPE = porcine pancreatic elastase; SH = spontaneously hypertensive; SO2 = sulfur dioxide; TLC = total lung capacity

Human COPD is associated with chronic cigarette smoking and is characterized by coexistent diseases of emphysema and bronchitis.13 The disease syndrome also encompasses many other pathologic manifestations, such as inflammation, airway fibrosis, and pulmonary infections. These manifestations occur at relatively different levels in individuals, such that it is nearly impossible to denote any one proportional combination in defining COPD. Clinically, all of these pathologies are associated with a gradual and persistent decline in FEV1. The disease develops in only ∼ 10% of smokers. and yet 80 to 90% of COPD patients are current or past smokers, suggesting that genetic predisposition may play a role in the pathogenesis of the disease. Involvement of a number of host susceptibility factors/genes has been proposed to explain the predisposition to COPD.4 Because of the complexities of COPD, and the chronicity associated with its pathogenesis, no animal model has been developed to represent the multiple components of the disease. In addition, laboratory rodents seem to differ from humans with respect to their host responses, such that their potential to repair or regenerate lung tissue is higher and induced inflammation or infections are not sustained over a long period of time.56 A number of rodent models have been reported which exhibit at least one of the attributes of COPD (eg, emphysema or bronchitis).8 However, these chemically induced rodent models of emphysema or bronchitis lack critical pathobiological features of human COPD, such as persistent lung inflammation and infection. The purpose of this study was to combine emphysema and bronchitis together in the rat such that prior emphysema developed by elastase instillation would potentiate persistence of bronchitis induced by sulfur dioxide (SO2). We hypothesized that the combination of elastase treatment followed by SO2 exposure would result in COPD with sustained inflammation in the rat.

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