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Does Reduced α1-Antitrypsin Activity Explain the Link Between Cigarette Smoking and Idiopathic Pulmonary Fibrosis?*

Edward D. Chan, MD, FCCP; Annemarie H. Ralston, PhD; Leland Shapiro, MD
Author and Funding Information

*From the Division of Pulmonary Sciences and Critical Care Medicine (Dr. Chan), Department of Medicine, National Jewish Medical and Research Center, and Division of Infectious Disease (Dr. Shapiro), University of Colorado Health Sciences Center, Denver, CO; and the Holland Laboratory (Dr. Ralston), Plasma Derivatives Department, American Red Cross, Rockville, MD.

Correspondence to: Edward D. Chan, MD, FCCP, K613e, Goodman Building, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO; e-mail: chane@njc.org



Chest. 2001;120(1_suppl):S72-S74. doi:10.1378/chest.120.1_suppl.S72
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Cigarette smoking is a risk factor for idiopathic pulmonary fibrosis (IPF),1 a fibrotic lung disease characterized in the early stages by injury to the interstitial walls, followed by an inflammatory alveolitis and progressive fibrosis.2 Nitric oxide (NO) is a potent proinflammatory mediator that may contribute to the exudative injury that occurs in the early stages of IPF. Experimental evidence suggests that NO production from macrophages may enhance cell injury and inflammation associated with IPF,34 as well as the analogous pulmonary fibrosis associated with exposure to asbestos and bleomycin.56 α1-Antitrypsin (AAT), the most abundant endogenous serine protease inhibitor, possesses anti-inflammatory properties. AAT is present in the serum at concentrations of 1.5 to 3.5 mg/mL, but levels can increase up to four times in inflammatory states.9 Nagai and coworkers10 showed that intraperitoneal AAT administration reduced bleomycin-induced pulmonary fibrosis in hamsters. This protective AAT effect was not due to alteration in elastase activity, chemotaxis, or neutrophil superoxide generation. The mechanism of AAT protection against pulmonary fibrosis is unexplained. Because NO and AAT may play opposing roles in lung inflammation and fibrosis, we investigated the effects of AAT on NO expression induced by interferon (IFN)-γ plus lipopolysaccharide (LPS) in mouse macrophages.

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