Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2011, Article ID 407657, 5 pages
http://dx.doi.org/10.1155/2011/407657
Review Article

Role of Oxidants in Interstitial Lung Diseases: Pneumoconioses, Constrictive Bronchiolitis, and Chronic Tropical Pulmonary Eosinophilia

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

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.

Abstract

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 lavage in humans has recovered alveolar macrophages (AMs) in dust diseases and eosinophils in TPE that release increased amounts of oxidants in vitro. Interestingly, TPE has massively increased eosinophils in the acute form and after treatment can still have ongoing eosinophilic inflammation. A course of prednisone for one week can reduce the oxidant burden and attendant inflammation and may be a strategy to prevent chronic TPE and interstitial lung disease.