Alcohol and lung injury and immunity

Samantha M. Yeligar, Michael M. Chen, Elizabeth J. Kovacs, Joseph Harold Sisson, Ellen L. Burnham, Lou Ann S Brown

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Annually, excessive alcohol use accounts for more than $220 billion in economic costs and 80,000 deaths, making excessive alcohol use the third leading lifestyle-related cause of death in the US. Patients with an alcohol-use disorder (AUD) also have an increased susceptibility to respiratory pathogens and lung injury, including a 2–4-fold increased risk of acute respiratory distress syndrome (ARDS). This review investigates some of the potential mechanisms by which alcohol causes lung injury and impairs lung immunity. In intoxicated individuals with burn injuries, activation of the gut-liver axis drives pulmonary inflammation, thereby negatively impacting morbidity and mortality. In the lung, the upper airway is the first checkpoint to fail in microbe clearance during alcohol-induced lung immune dysfunction. Brief and prolonged alcohol exposure drive different post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify novel alcohol targets and post-translational modifications in airway cilia that are involved in alcohol-dependent signal transduction pathways. When the upper airway fails to clear inhaled pathogens, they enter the alveolar space where they are primarily cleared by alveolar macrophages (AM). With chronic alcohol ingestion, oxidative stress pathways in the AMs are stimulated, thereby impairing AM immune capacity and pathogen clearance. The epidemiology of pneumococcal pneumonia and AUDs is well established, as both increased predisposition and illness severity have been reported. AUD subjects have increased susceptibility to pneumococcal pneumonia infections, which may be due to the pro-inflammatory response of AMs, leading to increased oxidative stress.

Original languageEnglish (US)
Pages (from-to)51-59
Number of pages9
JournalAlcohol
Volume55
DOIs
StatePublished - Sep 1 2016

Fingerprint

immunity
Lung Injury
Immunity
alcohol
Alcohols
Pathogens
Pneumococcal Pneumonia
Oxidative stress
Cilia
Alveolar Macrophages
Post Translational Protein Processing
Lung
Oxidative Stress
Pneumococcal Infections
Signal transduction
Epidemiology
Adult Respiratory Distress Syndrome
epidemiology
cause of death
Liver

Keywords

  • Airway cilia
  • Alcohol
  • Alveolar macrophage
  • Gut-liver-lung axis
  • Lung immunity
  • Lung injury

ASJC Scopus subject areas

  • Health(social science)
  • Biochemistry
  • Toxicology
  • Neurology
  • Behavioral Neuroscience

Cite this

Yeligar, S. M., Chen, M. M., Kovacs, E. J., Sisson, J. H., Burnham, E. L., & Brown, L. A. S. (2016). Alcohol and lung injury and immunity. Alcohol, 55, 51-59. https://doi.org/10.1016/j.alcohol.2016.08.005

Alcohol and lung injury and immunity. / Yeligar, Samantha M.; Chen, Michael M.; Kovacs, Elizabeth J.; Sisson, Joseph Harold; Burnham, Ellen L.; Brown, Lou Ann S.

In: Alcohol, Vol. 55, 01.09.2016, p. 51-59.

Research output: Contribution to journalReview article

Yeligar, SM, Chen, MM, Kovacs, EJ, Sisson, JH, Burnham, EL & Brown, LAS 2016, 'Alcohol and lung injury and immunity', Alcohol, vol. 55, pp. 51-59. https://doi.org/10.1016/j.alcohol.2016.08.005
Yeligar SM, Chen MM, Kovacs EJ, Sisson JH, Burnham EL, Brown LAS. Alcohol and lung injury and immunity. Alcohol. 2016 Sep 1;55:51-59. https://doi.org/10.1016/j.alcohol.2016.08.005
Yeligar, Samantha M. ; Chen, Michael M. ; Kovacs, Elizabeth J. ; Sisson, Joseph Harold ; Burnham, Ellen L. ; Brown, Lou Ann S. / Alcohol and lung injury and immunity. In: Alcohol. 2016 ; Vol. 55. pp. 51-59.
@article{7ea59b8deb644c29a0d0d51f36ede681,
title = "Alcohol and lung injury and immunity",
abstract = "Annually, excessive alcohol use accounts for more than $220 billion in economic costs and 80,000 deaths, making excessive alcohol use the third leading lifestyle-related cause of death in the US. Patients with an alcohol-use disorder (AUD) also have an increased susceptibility to respiratory pathogens and lung injury, including a 2–4-fold increased risk of acute respiratory distress syndrome (ARDS). This review investigates some of the potential mechanisms by which alcohol causes lung injury and impairs lung immunity. In intoxicated individuals with burn injuries, activation of the gut-liver axis drives pulmonary inflammation, thereby negatively impacting morbidity and mortality. In the lung, the upper airway is the first checkpoint to fail in microbe clearance during alcohol-induced lung immune dysfunction. Brief and prolonged alcohol exposure drive different post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify novel alcohol targets and post-translational modifications in airway cilia that are involved in alcohol-dependent signal transduction pathways. When the upper airway fails to clear inhaled pathogens, they enter the alveolar space where they are primarily cleared by alveolar macrophages (AM). With chronic alcohol ingestion, oxidative stress pathways in the AMs are stimulated, thereby impairing AM immune capacity and pathogen clearance. The epidemiology of pneumococcal pneumonia and AUDs is well established, as both increased predisposition and illness severity have been reported. AUD subjects have increased susceptibility to pneumococcal pneumonia infections, which may be due to the pro-inflammatory response of AMs, leading to increased oxidative stress.",
keywords = "Airway cilia, Alcohol, Alveolar macrophage, Gut-liver-lung axis, Lung immunity, Lung injury",
author = "Yeligar, {Samantha M.} and Chen, {Michael M.} and Kovacs, {Elizabeth J.} and Sisson, {Joseph Harold} and Burnham, {Ellen L.} and Brown, {Lou Ann S}",
year = "2016",
month = "9",
day = "1",
doi = "10.1016/j.alcohol.2016.08.005",
language = "English (US)",
volume = "55",
pages = "51--59",
journal = "Alcohol",
issn = "0741-8329",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Alcohol and lung injury and immunity

AU - Yeligar, Samantha M.

AU - Chen, Michael M.

AU - Kovacs, Elizabeth J.

AU - Sisson, Joseph Harold

AU - Burnham, Ellen L.

AU - Brown, Lou Ann S

PY - 2016/9/1

Y1 - 2016/9/1

N2 - Annually, excessive alcohol use accounts for more than $220 billion in economic costs and 80,000 deaths, making excessive alcohol use the third leading lifestyle-related cause of death in the US. Patients with an alcohol-use disorder (AUD) also have an increased susceptibility to respiratory pathogens and lung injury, including a 2–4-fold increased risk of acute respiratory distress syndrome (ARDS). This review investigates some of the potential mechanisms by which alcohol causes lung injury and impairs lung immunity. In intoxicated individuals with burn injuries, activation of the gut-liver axis drives pulmonary inflammation, thereby negatively impacting morbidity and mortality. In the lung, the upper airway is the first checkpoint to fail in microbe clearance during alcohol-induced lung immune dysfunction. Brief and prolonged alcohol exposure drive different post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify novel alcohol targets and post-translational modifications in airway cilia that are involved in alcohol-dependent signal transduction pathways. When the upper airway fails to clear inhaled pathogens, they enter the alveolar space where they are primarily cleared by alveolar macrophages (AM). With chronic alcohol ingestion, oxidative stress pathways in the AMs are stimulated, thereby impairing AM immune capacity and pathogen clearance. The epidemiology of pneumococcal pneumonia and AUDs is well established, as both increased predisposition and illness severity have been reported. AUD subjects have increased susceptibility to pneumococcal pneumonia infections, which may be due to the pro-inflammatory response of AMs, leading to increased oxidative stress.

AB - Annually, excessive alcohol use accounts for more than $220 billion in economic costs and 80,000 deaths, making excessive alcohol use the third leading lifestyle-related cause of death in the US. Patients with an alcohol-use disorder (AUD) also have an increased susceptibility to respiratory pathogens and lung injury, including a 2–4-fold increased risk of acute respiratory distress syndrome (ARDS). This review investigates some of the potential mechanisms by which alcohol causes lung injury and impairs lung immunity. In intoxicated individuals with burn injuries, activation of the gut-liver axis drives pulmonary inflammation, thereby negatively impacting morbidity and mortality. In the lung, the upper airway is the first checkpoint to fail in microbe clearance during alcohol-induced lung immune dysfunction. Brief and prolonged alcohol exposure drive different post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify novel alcohol targets and post-translational modifications in airway cilia that are involved in alcohol-dependent signal transduction pathways. When the upper airway fails to clear inhaled pathogens, they enter the alveolar space where they are primarily cleared by alveolar macrophages (AM). With chronic alcohol ingestion, oxidative stress pathways in the AMs are stimulated, thereby impairing AM immune capacity and pathogen clearance. The epidemiology of pneumococcal pneumonia and AUDs is well established, as both increased predisposition and illness severity have been reported. AUD subjects have increased susceptibility to pneumococcal pneumonia infections, which may be due to the pro-inflammatory response of AMs, leading to increased oxidative stress.

KW - Airway cilia

KW - Alcohol

KW - Alveolar macrophage

KW - Gut-liver-lung axis

KW - Lung immunity

KW - Lung injury

UR - http://www.scopus.com/inward/record.url?scp=84989315269&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84989315269&partnerID=8YFLogxK

U2 - 10.1016/j.alcohol.2016.08.005

DO - 10.1016/j.alcohol.2016.08.005

M3 - Review article

C2 - 27788778

AN - SCOPUS:84989315269

VL - 55

SP - 51

EP - 59

JO - Alcohol

JF - Alcohol

SN - 0741-8329

ER -