Alcohol abuse is a systemic disorder and increases the risk of lung injury. After ingestion, alcohol freely diffuses from the bronchial circulation directly through the ciliated epithelium where it vaporizes as it moves into the conducting airways. Some of vaporized alcohol can deposit back into the airway lining fluid and results in repeated exposure of the airway epithelium to high local concentrations of alcohol. Chronic alcohol ingestion is associated with increased renin-angiotensin system, induces oxidative stress through angiotensin (Ang) II stimulated NADPH oxidase expression and activity, and superoxide production. Alcohol metabolism within the lung through the cytochrome P 450 system may also be sufficient to exert significant oxidative stress. Alcohol inhibits the expression of GM-CSF and impairs immune system. Chronic ingestion of ethanol altered cellular functions and viability such as decreased surfactant processing, decreased barrier integrity, increased sensitivity to cytotoxin-induced apoptosis in vitro and in vivo in alveolar type II cells, and decreased phagocytosis of microorganisms in alveolar macrophages. The lung becomes more susceptible when a second hit such as sepsis occurs. Though dietary supplementation with glutathione precursors or selective Ang II type 2 receptor inhibition limits lung injury in animal model, the most attractive candidate for treating the alcoholic lung in the acute setting is recombinant GM-CSF. Whether any of these therapeutic strategies will prove to be effective in decreasing the consequences of alcohol abuse on acute pulmonary diseases is at present unknown.
Keywords: Alcohol, alveolar epithelial barrier, glutathione, lung, matrix metalloproteinases, mucocilliary clearance, oxidative stress, rennin-angiotensin system, transforming growth factor-beta, tumor necrosis factor-alpha
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