The effects of alcohol on immunity and bacterial infection in the lung

Gamble, Lisa; Mason, Carol M.; Nelson, Steve

doi:10.1016/j.medmal.2005.08.010

Cited by 52 publications

(39 citation statements)

References 30 publications

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“…Conversely, alcoholism was only found among TB patients, enabling the analysis for its potential repercussion on the in vitro immune response. In agreement with the reported effect of alcohol consumption on cell-mediated immune reactions [35] , our study documents that alcoholism may partly account for the depressed in vitro lymphoproliferation, indicating that its influence should be taken into account.…”

Section: Discussionsupporting

confidence: 92%

Impaired Immune Responses in Tuberculosis Patients Are Related to Weight Loss That Coexists with an Immunoendocrine Imbalance

Mahuad

Bozza

Pezzotto

et al. 2007

Neuroimmunomodulation

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The study’s objective was to examine whether factors related to the host status may bear some relation with the profile of the immune response displayed by tuberculosis (TB) patients. The in vitro immune response (antigen-driven lymphoproliferation and cytokine production) and the presence of alcoholism or disease-related factors, like heart and respiratory rates, and weight loss (body mass index, BMI) were investigated in 31 males with active, untreated TB. Compared to 16 age-matched healthy males, TB patients presented depressed lymphoproliferation and increased IL-10 and TGF-β production. Multivariate analysis indicated that most differences were no longer significant when controlling for the BMI. Immune and endocrine changes coexisting with weight loss, such as circulating levels of TNF-α, IFN-γ, IL-6, cortisol, dehydroepiandrosterone and thyroid hormones, were also analyzed. While pairwise correlations between serum levels of IFN-γ, T3 or T4 and BMI were not significant, BMI was negatively correlated with IL-6 levels (p < 0.025). In turn, levels of IL-6 correlated positively with cortisol concentrations (p <0.001). Stepwise regression analysis demonstrated that BMI was only associated with IL-6 (r = –0.423, R² = 0.18), with the difference remaining significant following adjustment for the other variables. As regards IL-6, BMI, cortisol and IFN-γ could explain 74% of variability in IL-6 concentrations (R² = 0.74). No evidence for effect modification was shown when performing adjusted calculations. To conclude, the relation between weight loss and abnormal immune response of TB patients is partly associated with the immunoendocrine imbalance observed in parallel.

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Section: Discussionsupporting

confidence: 92%

Impaired Immune Responses in Tuberculosis Patients Are Related to Weight Loss That Coexists with an Immunoendocrine Imbalance

Mahuad

Bozza

Pezzotto

et al. 2007

Neuroimmunomodulation

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“…When these processes are impaired or fail the particulate matter enters into the alveoli, evoking a self resolving inflammatory response by the alveolar macrophage (AM). Alcohol abuse perturbs the mucociliary clearance of the pathogens by cilia, the AM recognition and phagocytosis of the stimuli, generation of chemical mediators, and the recruitment of auxiliary defenses, as well as the secretion of surfactant by lung epithelial cells (D'Souza ElGuindy et al, 2007;D'Souza et al, 1996;Gamble et al, 2006;Joshi and Guidot, 2007;Szabo and Mandrekar, 2009;Wyatt et al, 2004). These adverse effects of acute and chronic alcohol intoxication on the lung have been reviewed extensively elsewhere (Boe´et al, 2009;Happel and Nelson, 2005).…”

Section: Lps-mediated Alcohol-induced Tissue Injurymentioning

confidence: 99%

“…Findings using in vivo animal models of acute alcohol intoxication and ⁄ or in vitro exposure of isolated AM to alcohol indicate that a single exposure to intoxicating levels (acute) of alcohol can suppress lung innate immune responses to acute immune stimulus. Studies performed using either lungs or immune cells isolated from human and rodents suggest that acute alcohol can suppress innate immune responses by altering the balance between pro-and anti-inflammatory mediators Gamble et al, 2006;Szabo and Mandrekar, 2009). It is suspected that alcohol inhibits inflammatory cytokine secretion by affecting the NF-jB signaling pathway (Happel and Nelson, 2005).…”

Section: Alcohol Modulates Immune Response During Bacterial and Viralmentioning

confidence: 99%

“…ROS produced during alcohol metabolism leads to inflammation mainly through TNF-a and TGF-b and cause cell death in the liver, lung, pancreas, heart and the brain. In addition, alcohol modulates local innate and adaptive immune responses (Neuman et al, 1993(Neuman et al, , 1998) that can alter resistance to a number of bacterial (Gamble et al, 2006;Szabo and Mandrekar, 2009) and viral (Graham, 2006;Neuman et al, 2008;Samet et al, 2003) infectious agents. Factors such as bacterial and viral infections enhance the inflammation and the deleterious effects of alcohol.…”

mentioning

confidence: 99%

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Alcohol, Signaling, and ECM Turnover

Seth

El-Guindy

Apte

et al. 2009

Alcoholism Clin & Exp Res

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Alcohol is recognized as a direct hepatotoxin, but the precise molecular pathways that are important for the initiation and progression of alcohol-induced tissue injury are not completely understood. The current understanding of alcohol toxicity to organs suggests that alcohol initiates injury by generation of oxidative and nonoxidative ethanol metabolites and via translocation of gut-derived endotoxin. These processes lead to cellular injury and stimulation of the inflammatory responses mediated through a variety of molecules. With continuing alcohol abuse, the injury progresses through impairment of tissue regeneration and extracellular matrix (ECM) turnover, leading to fibrogenesis and cirrhosis. Several cell types are involved in this process, the predominant being stellate cells, macrophages, and parenchymal cells. In response to alcohol, growth factors and cytokines activate many signaling cascades that regulate fibrogenesis. This mini-review brings together research focusing on the underlying mechanisms of alcohol-mediated injury in a number of organs. It highlights the various processes and molecules that are likely involved in inflammation, immune modulation, susceptibility to infection, ECM turnover and fibrogenesis in the liver, pancreas, and lung triggered by alcohol abuse.

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“…Alcoholism also affects adversely the T-and B-lymphocytes, which mediate the immune response against specific microorganisms and long term immunity (Szabo, 1999). *Corresponding author: Tel: +2348037147006;E-mail: chimn2004@yahoo.com Reports on alcohol induced immune dysfunction in humans and animal models abound (Szabo, 1999;Diaz et al, 2002;Gamble et al, 2006). Inspite of these reports, the extent to which alcohol suppresses immunity has not been quantified.…”

Section: Introductionmentioning

confidence: 99%