Abstract
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.
Highlights
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
It is a serious condition that occurs in critically ill patients alongside infection, injury, and uid accumulation in the lung that hinders effective oxygen exchange. e role of alcohol abuse in the development of ARDS was established in a clinical study involving 351 medical and intensive care unit patients at university-affiliated city hospitals [1,2,3]
Because chronic ethanol ingestion impacts all aspects of the alveolar epithelium, it is important to continue to study the consequence of alcohol abuse on all the cells that make up the alveolar airspace
Summary
E role of alcohol abuse in the development of ARDS was established in a clinical study involving 351 medical and intensive care unit patients at university-affiliated city hospitals [1,2,3]. Speaking, alveolar macrophages (AMs) may be considered the third cell type comprising the alveoli (alongside type 1 and type 2 cells). Previous studies have shown that chronic ethanol ingestion results in impaired alveolar macrophage function (i.e., decreased phagocytosis and increased reactive oxygen species production) via altered Nadph oxidase activity [11, 12]. Because chronic ethanol ingestion impacts all aspects of the alveolar epithelium, it is important to continue to study the consequence of alcohol abuse on all the cells that make up the alveolar airspace
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
