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BioMed Research International
Volume 2013, Article ID 470217, 7 pages
Review Article

Chronic Alcohol Ingestion Changes the Landscape of the Alveolar Epithelium

1Department of Pediatrics, Emory-Children Center for Developmental Lung Biology, 2015 Uppergate Drive, Suite 316K, Atlanta, GA 30322, USA
2The Nell Hodgson Woodruff School of Nursing, Atlanta, GA 30322, USA
3Emory Alcohol and Lung Biology Center, Atlanta, GA 30322, USA

Received 13 August 2012; Accepted 3 October 2012

Academic Editor: Y. James Kang

Copyright © 2013 Charles A. Downs et al. 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.


Similar to effects of alcohol on the heart, liver, and brain, the effects of ethanol (EtOH) on lung injury are preventable. Unlike other vital organ systems, however, the lethal effects of alcohol on the lung are underappreciated, perhaps because there are no signs of overt pulmonary disorder until a secondary insult, such as a bacterial infection or injury, occurs in the lung. This paper provides overview of the complex changes in the alveolar environment known to occur following both chronic and acute alcohol exposures. Contemporary animal and cell culture models for alcohol-induced lung dysfunction are discussed, with emphasis on the effect of alcohol on transepithelial transport processes, namely, epithelial sodium channel activity (ENaC). The cascading effect of tissue and phagocytic Nadph oxidase (Nox) may be triggered by ethanol exposure, and as such, alcohol ingestion and exposure lead to a prooxidative environment; thus impacting alveolar macrophage (AM) function and oxidative stress. A better understanding of how alcohol changes the landscape of the alveolar epithelium can lead to improvements in treating acute respiratory distress syndrome (ARDS) for which hospitalized alcoholics are at an increased risk.