The alcoholic lung disease: Historical background and clinical features

Karkoulias, Kiriakos; Tsitsaras, Haralampos; Patouchas, Dimitrios; Sampsonas, Fotios; Likouras, Dimostenis; Kaparianos, A; Spiropoulos, Kostas

doi:10.3390/medicina44090084

Cited by 6 publications

(8 citation statements)

References 77 publications

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“…Indirectly, alcohol and its metabolites may damage the endocrine system and disrupt the actions of hormones like cortisol, testosterone, growth hormone, and prolactin which, in turn, may affect pulmonary function or the function of related organs. For example, both alcohol and its metabolic products have been shown to interfere with glucose and lipid metabolism [ 90 , 92 ].…”

Section: Alcohol and Mechanisms Of Lung Injurymentioning

confidence: 99%

Potential Role of the Gut/Liver/Lung Axis in Alcohol-Induced Tissue Pathology

et al. 2015

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Both Alcoholic Liver Disease (ALD) and alcohol-related susceptibility to acute lung injury are estimated to account for the highest morbidity and mortality related to chronic alcohol abuse and, thus, represent a focus of intense investigation. In general, alcohol-induced derangements to both organs are considered to be independent and are often evaluated separately. However, the liver and lung share many general responses to damage, and specific responses to alcohol exposure. For example, both organs possess resident macrophages that play key roles in mediating the immune/inflammatory response. Additionally, alcohol-induced damage to both organs appears to involve oxidative stress that favors tissue injury. Another mechanism that appears to be shared between the organs is that inflammatory injury to both organs is enhanced by alcohol exposure. Lastly, altered extracellular matrix (ECM) deposition appears to be a key step in disease progression in both organs. Indeed, recent studies suggest that early subtle changes in the ECM may predispose the target organ to an inflammatory insult. The purpose of this chapter is to review the parallel mechanisms of liver and lung injury in response to alcohol consumption. This chapter will also explore the potential that these mechanisms are interdependent, as part of a gut-liver-lung axis.

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Section: Alcohol and Mechanisms Of Lung Injurymentioning

confidence: 99%

Potential Role of the Gut/Liver/Lung Axis in Alcohol-Induced Tissue Pathology

et al. 2015

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“…Alcohol abuse alone does not cause acute lung injury though it does increase risk for infection and acute respiratory distress syndrome (Guidot & Hart, 2005). Damage due to concurrent drug and tobacco use is often indistinguishable (Karkoulias et al, 2008) but can be additive (Fligiel et al, 1997). Future research should identify the extent to which clients in drug treatment have respiratory problems, the degree to which respiratory problems are attributable to tobacco or other drug use, and whether quitting smoking helps ameliorate these problems.…”

Section: Resultsmentioning

confidence: 99%

Understanding the drug treatment community's ambivalence towards tobacco use and treatment

Richter

Hunt

Cupertino

et al. 2012

International Journal of Drug Policy

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Background Most clients in drug treatment smoke cigarettes, but few facilities provide treatment for tobacco dependence. We identify subjective experiences and social processes that may influence facility adoption of tobacco treatment policies and practices. Methods Cross-sectional, semi-structured interviews were conducted with staff, directors and clients of 8 drug treatment facilities in the Midwestern U.S. We assembled a purposive sample stratified by ownership, methadone provision, and treatment service provision. We conducted in-person interviews with clinic directors and 54 staff and clients and employed a mixed-method analytic approach. Results Facility policies and philosophy related to tobacco differed from those regarding alcohol and other drugs. Participants suggested facilities may not treat tobacco dependence because it does not create legal and social problems that force clients into treatment. Tobacco dependence treatment falls outside of a core function of drug treatment, which is to help clients fix legal problems caused by their drug use. Moreover, proactively treating clients for tobacco dependence creates strong ambivalence among staff and directors. On the one hand, staff smoking would violate core principles of drug treatment (i.e., the importance of staff abstinence from drugs of abuse); on the other, staff who smoke feel their personal rights and jobs are threatened. This situation creates strong incentives for staff to resist adoption of tobacco dependence treatment. Unlike other studies, the fear of jeopardizing clients’ abstinence from other drugs did not emerge as a downside for treating tobacco dependence. Conclusions International and national trends will probably increase the pressure to treat tobacco dependence during drug treatment. However, the U.S. context of drug treatment, as a patchwork, under-funded industry with high employee turnover, may undermine true adoption. At present, many facility staff resolve their ambivalence by reporting they “offer” treatment, but actually providing none. To facilitate dissemination of service provision, it may be useful to identify incentives for U.S. facilities that are closely aligned with the criminal justice system, help facilities define policies and treatment roles for staff who smoke, and better define the role of facilities in preventing morbidity and mortality.

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“…Alcohol abuse is common in all social classes in the world [ 1 ]. Chronic consumption or acute excessive consumption of alcohol is harmful for important organs including the lung [ 2 ]. Although the absorbed alcohol is mainly metabolized in the liver, the unmetabolized portion enters the circulation and via pulmonary vessels reaches the lung where it affects its homeostasis or causes injury of local tissue [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…Although the absorbed alcohol is mainly metabolized in the liver, the unmetabolized portion enters the circulation and via pulmonary vessels reaches the lung where it affects its homeostasis or causes injury of local tissue [ 3 ]. It has been reported that the inhalation of alcohol compromises lung epithelial barrier function and induces lung edema [ 2 ]. The mechanism is not fully understood yet.…”

Section: Introductionmentioning

confidence: 99%

“…Since alcoholism affects the epithelial barrier integrity [ 2 ], and since Mφ-derived TNF is one of the factors inducing epithelial barrier dysfunction [ 7 ], and depression of A20 can strengthen the expression of TNF in Mφ [ 6 ], we hypothesized that chronic alcohol consumption induces lung endothelial barrier dysfunction via modulating the A20 and TNF expression in Mφ. The hypothesis was tested in this study with a mouse model, observing step by step the expression of A20 and TNF in lung Mφ and lung endothelial barrier function.…”

Section: Introductionmentioning

confidence: 99%

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Chronic ingestion of alcohol modulates expression of ubiquitin editing enzyme A20 in lung macrophages

Huang

Chen

Liu

2011

Multidisciplinary Respiratory Medicine

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BackgroundAlcohol abuse is involved in the pathogenesis of multiple organ disorders; the underlying mechanism is incompletely understood. The ubiquitin editing enzyme A20 is involved in regulating activities in the cell. Suppression of A20 is suggested as one factor in the initiation of inflammation. This study investigates the mechanism by which chronic alcohol consumption modulates the levels of ubiquitin editing enzyme A20 in macrophages and further contributes to induce endothelial barrier dysfunction in the lung.MethodsMice were gavage-fed with 40% alcohol daily for 0-3 weeks. Airway macrophages were collected by lung lavage. Expression of ubiquitin editing enzyme A20 in isolated macrophages was assessed at both mRNA and protein levels. The endothelial barrier function of the lung was evaluated by the Evans blue method.ResultsMice treated with alcohol for 3 weeks showed an increase in cell infiltration in the lung in response to exposure to peptidoglycan; over 80% of the infiltrated cells were macrophages. Furthermore, we observed that A20 level was suppressed in macrophages of mice treated with alcohol; the levels of tumor necrosis factor, interleukin-6 and nuclear factor kappa B in macrophage were increased. In addition, the endothelial barrier function of the lung was compromised, showing excessive infiltration of Evans blue in the lung indicating lung edema. Pretreatment with synthesized A20 inhibited alcohol-induced lung endothelial barrier dysfunction.ConclusionsWe conclude that chronic alcohol ingestion disturbs the endothelial barrier function in the lung by modulating macrophage properties. Increase in A20 in the cell may have potential for the treatment of inflammatory disorders.

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The alcoholic lung disease: Historical background and clinical features

Cited by 6 publications

References 77 publications

Potential Role of the Gut/Liver/Lung Axis in Alcohol-Induced Tissue Pathology

Potential Role of the Gut/Liver/Lung Axis in Alcohol-Induced Tissue Pathology

Understanding the drug treatment community's ambivalence towards tobacco use and treatment

Chronic ingestion of alcohol modulates expression of ubiquitin editing enzyme A20 in lung macrophages

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