Impact of Alcohol Abuse in the Etiology and Severity of Community-Acquired Pneumonia

Roux, A de; Cavalcanti, Manuela; Marcos, María Ángeles; García, Elisa; Ewig, Santiago; Mensa, José; Torres, Antoni

doi:10.1378/chest.129.5.1219

Cited by 144 publications

(121 citation statements)

References 27 publications

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“…For example, chronic alcoholics have an increased incidence and higher mortality rate related to bacterial pneumonia (de Roux et al, 2006;elEbiary et al, 1997;Jong et al, 1995) and a three-fold increase in incidence of infection and sepsis after surgery (von Dossow et al, 2004). In HIV patients, concurrent alcohol consumption increases the susceptibility to various infections (Justice et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Lazic¹,

Wyatt²,

Matić³

et al. 2007

Alcohol

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In addition to neurodevelopmental effects, alcohol consumption at high levels during pregnancy is associated with immunomodulation and premature birth. Premature birth, in turn, is associated with increased susceptibility to various infectious agents such as Respiratory Syncytial Virus (RSV). The initial line of pulmonary innate defense includes the mucociliary apparatus, which expels microorganisms trapped within the airway secretions. Surfactant proteins A and D (SP-A and SP-D, respectively) are additional components of pulmonary innate immunity and have an important role in pulmonary defense against inhaled pathogens. The purpose of this study was to determine if chronic alcohol consumption during the third trimester of pregnancy alters the function of the mucociliary apparatus and expression of SP-A and SP-D of fetal lung epithelia. Sixteen, date-mated ewes were assigned to two different groups; an ethanol exposed group in which ewes received ethanol through surgically implanted intra-abomasal cannula during the third trimester of pregnancy, and a control group in which ewes received the equivalent amount of water instead of ethanol. Within these two groups, ewes were further randomly assigned to a full-term group in which the lambs were naturally delivered, and a pre-term group in which the lambs were delivered prematurely via an abdominal incision and uterotomy. Ethanol was administered 5 times a week as a 40% solution at 1gr/kg of body weight. The mean maternal serum alcohol concentration (SAC) measured 6 hr post administration was 16.3 +/− 4.36 mg/dL. Tracheas from 6 full-term lambs were collected to assess ciliary beat frequency (CBF). The lung tissue from all (24) lambs was collected for immunohistochemistry (IHC) analysis of SP-A and SP-D protein production and fluorogenic realtime quantitative polymerase chain reaction analysis (qPCR) of SP-A and SP-D mRNA levels. Exposure to ethanol during pregnancy significantly blocked stimulated increase in CBF though ethanol-mediated desensitization of cAMP-dependant protein kinase (PKA). In addition, pre-term born/ethanol-exposed lambs showed significantly decreased SP-A m-RNA expression when compared to the pre-term born/control group (p=0.004); no significant changes were seen with SP-D. The full-term/ethanol exposed lambs had no significant alterations in mRNA levels, but had significantly less detectable SP-A protein when compared to the full-term/control lambs (p=0.02).Corresponding author: Tatjana Lazic, DVM, MS, 2740 Veterinary Medicine, Department of Veterinary Pathology, Iowa State University, Ames, Iowa 50011-1250, 515-294-6688, FAX 515-294-5423, tlazic@iastate.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process error...

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Section: Discussionmentioning

confidence: 99%

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Lazic¹,

Wyatt²,

Matić³

et al. 2007

Alcohol

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“…8 Only one Level 3 social factor, being a nursing home resident, significantly increased the odds of mortality (OR=1.5). 24 The use of alcohol, 30,31 distance to hospital 32 and urban neighborhood 20 were examined but not significantly associated with increased mortality. Table 5 shows the social factors that were examined in relation to readmissions in HF.…”

Section: Social Factors Associated With Mortality In Pneumoniamentioning

confidence: 99%

Impact of Social Factors on Risk of Readmission or Mortality in Pneumonia and Heart Failure: Systematic Review

et al. 2012

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“…Among these widespread effects, alcohol abuse renders individuals susceptible to pulmonary infections and acute lung injury (7)(8)(9)(10). We have explored potential mechanisms in experimental animal models and determined that chronic alcohol ingestion causes previously unrecognized cellular dysfunction and oxidative stress, as best reflected by significant decreases in glutathione (GSH) levels, within the alveolar space (11)(12)(13)(14).…”

mentioning

confidence: 99%

Alcoholism Causes Alveolar Macrophage Zinc Deficiency and Immune Dysfunction

Mehta

Yeligar

Elon

et al. 2013

Am J Respir Crit Care Med

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Rationale: Alcohol use disorders cause oxidative stress in the lower airways and increase susceptibility to pneumonia and lung injury. Currently, no therapeutic options exist to mitigate the pulmonary consequences of alcoholism. Objectives: We recently determined in an animal model that alcohol ingestion impairs pulmonary zinc metabolism and causes alveolar macrophage immune dysfunction. The objective of this research is to determine the effects of alcoholism on zinc bioavailability and alveolar macrophage function in human subjects. Methods: We recruited otherwise healthy alcoholics (n ¼ 17) and matched control subjects (n ¼ 17) who underwent bronchoscopy for isolation of alveolar macrophages, which were analyzed for intracellular zinc, phagocytic function, and surface expression of granulocyte-macrophage colony-stimulating factor receptor; all three of these indices are decreased in experimental models. Measurements and Main Results: Alcoholic subjects had normal serum zinc, but significantly decreased alveolar macrophage intracellular zinc levels (adjusted means [SE] Conclusions: These novel clinical findings provide evidence that alcohol abuse is associated with significant zinc deficiency and immune dysfunction within the alveolar space and suggest that dietary supplementation with zinc and glutathione precursors could enhance airway innate immunity and decrease the risk for pneumonia or lung injury in these vulnerable individuals.Keywords: alcohol abuse; alveolar macrophage; zinc; immunity; glutathione Alcohol use and abuse are prevalent and impose significant health burdens in society. A recent national survey suggests that more than half of the population in the United States older than the age of 12 consumes alcohol (1) and the lifetime prevalence of alcohol abuse is 18% (2). Tragically, alcohol abuse is the third leading cause of preventable death in the United States (3), and alcoholism is associated with numerous chronic, nonfatal health implications. The overall annual cost of alcohol abuse to American society has been estimated to be upward of $200 billion (4).The consequences of alcoholism span multiple organ systems, including the heart, liver, brain, and skeletal muscle (5, 6). Among these widespread effects, alcohol abuse renders individuals susceptible to pulmonary infections and acute lung injury (7-10). We have explored potential mechanisms in experimental animal models and determined that chronic alcohol ingestion causes previously unrecognized cellular dysfunction and oxidative stress, as best reflected by significant decreases in glutathione (GSH) levels, within the alveolar space (11-14). Alveolar macrophages, which are the primary immune cell in the lower airways, exhibit impaired phagocytosis and respiratory burst generation in animal models of chronic alcohol ingestion (15, 16), and treatment with antioxidants reverses these defects (17, 18). In addition, we established that decreased signaling of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates alcohol-induced alveo...

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Impact of Alcohol Abuse in the Etiology and Severity of Community-Acquired Pneumonia

Cited by 144 publications

References 27 publications

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Impact of Social Factors on Risk of Readmission or Mortality in Pneumonia and Heart Failure: Systematic Review

Alcoholism Causes Alveolar Macrophage Zinc Deficiency and Immune Dysfunction

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