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Alcoholic lung disease.

Kershaw CD, Guidot DM - Alcohol Res Health (2008)

Bottom Line: This translates to tens of thousands of excess deaths in the United States each year from alcohol-mediated lung injury, which is comparable to scarring of the liver (i.e., cirrhosis) in terms of alcohol-related mortality.However, there have been no systems biological approaches to the study of the alcoholic lung to date.However, the alcoholic lung represents a clear example of environment-host interactions that should be well suited for such applications.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University School of Medicine, Atlanta, Georgia.

ABSTRACT
In addition to its well-known association with lung infection (i.e., pneumonia), alcohol abuse now is recognized as an independent factor that increases by three- to four-fold the incidence of the acute respiratory distress syndrome, a severe form of acute lung injury with a mortality rate of 40 to 50 percent. This translates to tens of thousands of excess deaths in the United States each year from alcohol-mediated lung injury, which is comparable to scarring of the liver (i.e., cirrhosis) in terms of alcohol-related mortality. Experimental and clinical studies are shedding light on the basic mechanisms by which alcohol abuse predisposes some people to both acute lung injury and pneumonia. At the same time, novel therapeutic targets could be utilized in treating these uniquely vulnerable people. However, there have been no systems biological approaches to the study of the alcoholic lung to date. This is in part because the association between alcohol abuse and acute lung injury was made relatively recently and remains largely unrecognized, even by lung researchers. In parallel, efforts to study complex diseases such as acute lung injury and pneumonia using a genomics and/or proteomics approach, which involves the study of an organism's genes and/or proteins, still are in their infancy. However, the alcoholic lung represents a clear example of environment-host interactions that should be well suited for such applications.

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Related in: MedlinePlus

Schematic illustration of the mechanisms by which alcohol abuse increases the risk of the acute respiratory distress syndrome (ARDS). In addition to increasing the risk of developing acute illnesses that lead to ARDS, such as the entry of stomach secretions into the trachea and lungs (i.e., gastric aspiration), trauma, and severe pneumonia, alcohol abuse impairs the function of the lining of the lung’s air sacs (i.e., alveolar epithelium), thereby rendering the lung susceptible to injury from fluid accumulation (i.e., ARDS) that might not otherwise occur in a healthy person who experiences the same initial injury or infection.NOTE: Oxidative stress: damaging chemical imbalance in the cell. Surfactant: the substance that serves to maintain the stability of lung tissue by reducing the surface tension of fluids that coat the lung.
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f3-arh-31-1-66: Schematic illustration of the mechanisms by which alcohol abuse increases the risk of the acute respiratory distress syndrome (ARDS). In addition to increasing the risk of developing acute illnesses that lead to ARDS, such as the entry of stomach secretions into the trachea and lungs (i.e., gastric aspiration), trauma, and severe pneumonia, alcohol abuse impairs the function of the lining of the lung’s air sacs (i.e., alveolar epithelium), thereby rendering the lung susceptible to injury from fluid accumulation (i.e., ARDS) that might not otherwise occur in a healthy person who experiences the same initial injury or infection.NOTE: Oxidative stress: damaging chemical imbalance in the cell. Surfactant: the substance that serves to maintain the stability of lung tissue by reducing the surface tension of fluids that coat the lung.

Mentions: In summary, in addition to its well-known association with pneumonia, alcohol abuse independently increases the risk of ARDS two- to four-fold in at-risk individuals, and this is exacerbated by the fact that alcohol abuse also increases the risk for trauma, sepsis, and other acute illnesses that lead to ARDS. Although the pathological mechanisms by which alcohol abuse renders the lung susceptible to acute injury from fluid accumulation likely reflect multiple cellular functions within the lung, defects in the alveolar epithelium play a major role. In concert with these defects in alveolar epithelial function, alcohol-mediated suppression of alveolar macrophage immune functions are central to the increased risk for pneumonia. figure 3 shows a highly simplified illustration of how alcohol abuse increases the incidence of ARDS, by augmenting the chances of developing an at-risk diagnosis such as trauma and by impairing critical functions within the alveolar epithelium.


Alcoholic lung disease.

Kershaw CD, Guidot DM - Alcohol Res Health (2008)

Schematic illustration of the mechanisms by which alcohol abuse increases the risk of the acute respiratory distress syndrome (ARDS). In addition to increasing the risk of developing acute illnesses that lead to ARDS, such as the entry of stomach secretions into the trachea and lungs (i.e., gastric aspiration), trauma, and severe pneumonia, alcohol abuse impairs the function of the lining of the lung’s air sacs (i.e., alveolar epithelium), thereby rendering the lung susceptible to injury from fluid accumulation (i.e., ARDS) that might not otherwise occur in a healthy person who experiences the same initial injury or infection.NOTE: Oxidative stress: damaging chemical imbalance in the cell. Surfactant: the substance that serves to maintain the stability of lung tissue by reducing the surface tension of fluids that coat the lung.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3860447&req=5

f3-arh-31-1-66: Schematic illustration of the mechanisms by which alcohol abuse increases the risk of the acute respiratory distress syndrome (ARDS). In addition to increasing the risk of developing acute illnesses that lead to ARDS, such as the entry of stomach secretions into the trachea and lungs (i.e., gastric aspiration), trauma, and severe pneumonia, alcohol abuse impairs the function of the lining of the lung’s air sacs (i.e., alveolar epithelium), thereby rendering the lung susceptible to injury from fluid accumulation (i.e., ARDS) that might not otherwise occur in a healthy person who experiences the same initial injury or infection.NOTE: Oxidative stress: damaging chemical imbalance in the cell. Surfactant: the substance that serves to maintain the stability of lung tissue by reducing the surface tension of fluids that coat the lung.
Mentions: In summary, in addition to its well-known association with pneumonia, alcohol abuse independently increases the risk of ARDS two- to four-fold in at-risk individuals, and this is exacerbated by the fact that alcohol abuse also increases the risk for trauma, sepsis, and other acute illnesses that lead to ARDS. Although the pathological mechanisms by which alcohol abuse renders the lung susceptible to acute injury from fluid accumulation likely reflect multiple cellular functions within the lung, defects in the alveolar epithelium play a major role. In concert with these defects in alveolar epithelial function, alcohol-mediated suppression of alveolar macrophage immune functions are central to the increased risk for pneumonia. figure 3 shows a highly simplified illustration of how alcohol abuse increases the incidence of ARDS, by augmenting the chances of developing an at-risk diagnosis such as trauma and by impairing critical functions within the alveolar epithelium.

Bottom Line: This translates to tens of thousands of excess deaths in the United States each year from alcohol-mediated lung injury, which is comparable to scarring of the liver (i.e., cirrhosis) in terms of alcohol-related mortality.However, there have been no systems biological approaches to the study of the alcoholic lung to date.However, the alcoholic lung represents a clear example of environment-host interactions that should be well suited for such applications.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University School of Medicine, Atlanta, Georgia.

ABSTRACT
In addition to its well-known association with lung infection (i.e., pneumonia), alcohol abuse now is recognized as an independent factor that increases by three- to four-fold the incidence of the acute respiratory distress syndrome, a severe form of acute lung injury with a mortality rate of 40 to 50 percent. This translates to tens of thousands of excess deaths in the United States each year from alcohol-mediated lung injury, which is comparable to scarring of the liver (i.e., cirrhosis) in terms of alcohol-related mortality. Experimental and clinical studies are shedding light on the basic mechanisms by which alcohol abuse predisposes some people to both acute lung injury and pneumonia. At the same time, novel therapeutic targets could be utilized in treating these uniquely vulnerable people. However, there have been no systems biological approaches to the study of the alcoholic lung to date. This is in part because the association between alcohol abuse and acute lung injury was made relatively recently and remains largely unrecognized, even by lung researchers. In parallel, efforts to study complex diseases such as acute lung injury and pneumonia using a genomics and/or proteomics approach, which involves the study of an organism's genes and/or proteins, still are in their infancy. However, the alcoholic lung represents a clear example of environment-host interactions that should be well suited for such applications.

Show MeSH
Related in: MedlinePlus