role of oxidants in interstitial lung diseases pneumoconioses, constrictive bronchiolitis, and chronic tropical pulmonary eosinophilia氧化剂在间质性肺疾病尘肺,紧缩细支气管炎,慢性热带肺嗜酸性粒细胞.pdf

Hindawi Publishing Corporation Mediators of Inflammation Volume 2011, Article ID 407657, 5 pages doi:10.1155/2011/407657 Review Article Role of Oxidants in Interstitial Lung Diseases: Pneumoconioses, Constrictive Bronchiolitis, and Chronic Tropical Pulmonary Eosinophilia William N. Rom Division of Pulmonary, Critical Care, and Sleep Medicine, Departments of Medicine and Environmental Medicine, New York University School of Medicine, New York, NY 10016, USA Correspondence should be addressed to William N. Rom, william.rom@ Received 7 July 2011; Accepted 23 August 2011 Academic Editor: Fulvio D’Acquisto Copyright © 2011 William N. Rom. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Oxidants such as superoxide anion, hydrogen peroxide, and myeloperoxidase from activated inflammatory cells in the lower respiratory tract contribute to inflammation and injury. Etiologic agents include inorganic particulates such as asbestos, silica, or coal mine dust or mixtures of inorganic dust and combustion materials found in World Trade Center dust and smoke. These etiologic agents are phagocytosed by alveolar macrophages or bronchial epithelial cells and release chemotactic factors that recruit inflammatory cells to the lung. Chemotactic factors attract and activate neutrophils, eosinophils, mast cells, and lymphocytes and further activate macrophages to release more oxidants. Inorganic dusts target alveolar macrophages, World Trade Center dust targets bronchial epithelial cells, and eosinophils characterize tropical pulmonary eosinophilia (TPE) caused by filarial organisms. The technique of bronchoalveolar lava