PMID- 27788778
OWN - NLM
STAT- MEDLINE
DCOM- 20180103
LR  - 20220317
IS  - 1873-6823 (Electronic)
IS  - 0741-8329 (Print)
IS  - 0741-8329 (Linking)
VI  - 55
DP  - 2016 Sep
TI  - Alcohol and lung injury and immunity.
PG  - 51-59
LID - S0741-8329(16)30074-X [pii]
LID - 10.1016/j.alcohol.2016.08.005 [doi]
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.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - Yeligar, Samantha M
AU  - Yeligar SM
AD  - Department of Medicine, Emory University and Atlanta Veterans Affairs Medical 
      Center, Decatur, GA 30033, USA.
FAU - Chen, Michael M
AU  - Chen MM
AD  - Burn and Shock Trauma Research Institute, Alcohol Research Program, Integrative 
      Cell Biology Program, Loyola University Chicago Stritch School of Medicine, 
      Maywood, IL 60153, USA.
FAU - Kovacs, Elizabeth J
AU  - Kovacs EJ
AD  - Department of Surgery, University of Colorado School of Medicine, Aurora, CO 
      80045, USA.
FAU - Sisson, Joseph H
AU  - Sisson JH
AD  - Pulmonary, Critical Care, Sleep and Allergy Division, Department of Internal 
      Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.
FAU - Burnham, Ellen L
AU  - Burnham EL
AD  - Department of Medicine, Division of Pulmonary Sciences and Critical Care 
      Medicine, University of Colorado School of Medicine, Aurora, CO 80045, USA.
FAU - Brown, Lou Ann S
AU  - Brown LA
AD  - Department of Pediatrics, Emory University, Atlanta, GA 30322, USA. Electronic 
      address: lbrow03@emory.edu.
LA  - eng
GR  - R01 AA012197/AA/NIAAA NIH HHS/United States
GR  - F30 AA024676/AA/NIAAA NIH HHS/United States
GR  - R01 AA008769/AA/NIAAA NIH HHS/United States
GR  - T32 AA013527/AA/NIAAA NIH HHS/United States
GR  - P50 AA013757/AA/NIAAA NIH HHS/United States
GR  - R00 AA021803/AA/NIAAA NIH HHS/United States
GR  - F30 AA022856/AA/NIAAA NIH HHS/United States
GR  - R01 AA012034/AA/NIAAA NIH HHS/United States
GR  - R01 GM115257/GM/NIGMS NIH HHS/United States
GR  - K99 AA021803/AA/NIAAA NIH HHS/United States
GR  - R24 AA019661/AA/NIAAA NIH HHS/United States
GR  - UL1 TR001082/TR/NCATS NIH HHS/United States
GR  - F32 AA019859/AA/NIAAA NIH HHS/United States
GR  - R21 AA023193/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20160916
PL  - United States
TA  - Alcohol
JT  - Alcohol (Fayetteville, N.Y.)
JID - 8502311
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Alcohol Drinking/adverse effects/*immunology
MH  - Animals
MH  - Ethanol/administration & dosage/*toxicity
MH  - Gastrointestinal Tract/drug effects/immunology
MH  - Humans
MH  - Immunity, Cellular/drug effects/*immunology
MH  - Lung Injury/chemically induced/*immunology
MH  - Macrophages, Alveolar/drug effects/immunology
MH  - Oxidative Stress/drug effects/immunology
PMC - PMC5319482
MID - NIHMS820826
OTO - NOTNLM
OT  - Airway cilia
OT  - Alcohol
OT  - Alveolar macrophage
OT  - Gut-liver-lung axis
OT  - Lung immunity
OT  - Lung injury
EDAT- 2016/10/30 06:00
MHDA- 2018/01/04 06:00
PMCR- 2017/09/16
CRDT- 2016/10/30 06:00
PHST- 2016/03/16 00:00 [received]
PHST- 2016/07/07 00:00 [revised]
PHST- 2016/08/24 00:00 [accepted]
PHST- 2016/10/30 06:00 [pubmed]
PHST- 2018/01/04 06:00 [medline]
PHST- 2016/10/30 06:00 [entrez]
PHST- 2017/09/16 00:00 [pmc-release]
AID - S0741-8329(16)30074-X [pii]
AID - 10.1016/j.alcohol.2016.08.005 [doi]
PST - ppublish
SO  - Alcohol. 2016 Sep;55:51-59. doi: 10.1016/j.alcohol.2016.08.005. Epub 2016 Sep 16.